Objective:To explore the role and mechanism of serum response factor (SRF) and lncRNA FGD5-AS1 in lung adenocarcinoma (LUAD).Methods:The plasma and tissue wax of LUAD patients treated in Tangshan People's Hospital from 2020 to 2022 and the plasma of healthy people were collected. The expression of SRF in LUAD tissues and cells, and the expression of lncRNA FGD5-AS1 in LUAD tissues, plasma and cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The expression levels of SRF and lncRNA FGD5-AS1 in LUAD tissue microarray were detected by immunohistochemistry and in situ hybridization. LUAD cells A549, H1299 and H1975 were cultured in vitro and divided into si-NC and si-SRF groups, si-NC and si-lncRNA FGD5-AS1 groups, pcDNA3.1 and lncRNA FGD5-AS1 groups, si-NC+pcDNA3.1/si-SRF+pcDNA3.1/si-SRF+lncRNA FGD5-AS1 groups. The effects of the above groups on the proliferation, invasion and migration of LUAD cells were detected by CCK-8, cloning formation, EdU, Transwell and scratch test. The JASPAR database was used to predict the downstream lncRNA FGD5-AS1 that can be regulated by SRF; double luciferase experiment, chromatin Immunoprecipitation (CHIP) and electrophoretic mobility shift assay (EMSA) experiment were used to verify the regulatory effect between SRF and lncRNA FGD5-AS1, and the subcutaneous tumorigenesis experiment in nude mice was used to detect the effects of cells that stably knock down SRF and stably overexpress lncRNA FGD5-AS1 on the growth of transplanted tumors. Results:The results of immunohistochemistry showed that the mean optical density of SRF in LUAD tissues (1.49±0.33) was higher than that in adjacent tissues (1.00±0.00, P＜0.001). The expression level of SRF in paraffin tissues of LUAD patients was higher than that in normal tissues adjacent to cancer ( P=0.037). CCK-8, cloning, scratch and Transwell experiments showed that knockdown SRF could inhibit the proliferation, migration and invasion of A549 and H1299 cells, respectively. [For A549 cells: The clone formation count, migration count, invasion count, and 48-h migration distance ratio were (233.70±18.50), (808.70±6.11), (489.70±53.00), and 1.00±0.03, respectively, in the si-NC group; and (131.30±22.50), (403.00±9.54), (372.70±26.27), and 2.14±0.09, respectively, in the si-SRF group. For H1299 cells: The clone formation count, migration count, invasion count, and 48-h migration distance ratio were (194.30±20.98), (988.70±64.52), (907.70±67.02), and 1.00±0.05, respectively, in the si-NC group; and (137.70±7.77), (665.70±157.10), (565.70±67.01), and 1.52±0.03, respectively, in the si-SRF group. All comparisons showed statistically significant differences ( P＜0.05)] JASPAR database prediction shows that SRF and lncRNA FGD5-AS1 have binding site. The double luciferase experiment, CHIP and EMSA experiments showed that SRF could regulate lncRNA FGD5-AS1. In situ hybridization showed that the mean optical density of lncRNA FGD5-AS1 in tissue microarray of LUAD patients (1.28±0.31) was higher than that in adjacent tissues (1.00±0.00, P＜0.001). The results of qRT-PCR experiment showed that the expression level of lncRNA FGD5-AS1 in wax tissues of LUAD patients was higher than that in normal tissues adjacent to cancer ( P=0.017). The expression level of lncRNA FGD5-AS1 in plasma of LUAD patients (3.48±2.62) was higher than that of healthy people (1.02±0.03, P＜0.001). CCK-8, cloning, EDU, scratch and Transwell experiments showed that overexpression of lncRNA FGD5-AS1 could promote cell proliferation [For A549 cells: The clone formation count, EdU-positive cell count, invasion count, and 48-h migration distance ratio were (22.67±5.86), (1.00±0.09), (135.70±13.20), and 0.35±0.02, respectively, in the pcDNA3.1 group; and (46.33±9.07), (1.65±0.10), (205.00±13.23), and 0.20±0.01, respectively, in the FGD5-AS1-overexpressing group. All comparisons showed statistically significant differences ( P＜0.05)], migration and invasion and vice versa [For H1975 cells: The clone formation count, EdU-positive cell count, invasion count, and 48-h migration distance ratio were (75.33±4.16), (1.00±0.02), (258.70±45.79), and 0.18±0.01, respectively, in the NC group; and (37.00±4.00), (0.52±0.07), (130.70±9.07), and 0.53±0.04, respectively, in the lncRNA FGD5-AS1 knockdown group (si-lncRNA FGD5-AS1 group). All comparisons showed statistically significant differences ( P＜0.05)]. Overexpression of lncRNA FGD5-AS1 could rescue the effect of knockdown SRF on the proliferation, migration and invasion of A549 and H1299 cells. The results of subcutaneous tumorigenesis experiment in nude mice indicated that the tumorigenicity of LUAD cells stably knockdown SRF was weakened and vice versa. Conclusion:SRF can promote the progress of LUAD by regulating lncRNA FGD5-AS1.

Objective To develop an innovative minimally invasive rotary-cutting surgical system for axillary osmidrosis,and conduct clinical validation.Methods The design concept,technical principles and system composition of the innovative minimally invasive rotary-cutting surgical system for axillary osmidrosis were introduced.A total of 73 patients(146 axillae)with axillary osmidrosis were enrolled as subjects,and underwent surgery using the newly developed surgical system.Clinical validation of the system was performed by evaluating postoperative scarring,odor elimination rate,postoperative complication incidence,and patient satisfaction.Results The study demonstrated favorable clinical outcomes in the following aspects:postoperative scarring,odor elimination rate,postoperative complication incidence,and patient satisfaction.Conclusion The minimally invasive rotary-cutting surgical system for axillary osmidrosis is rationally designed.The rotary-cutting puncture device is safe,effective,minimally invasive,and convenient for axillary osmidrosis surgery,warranting further clinical validation and widespread application.

Objective To develop an innovative minimally invasive rotary-cutting surgical system for axillary osmidrosis,and conduct clinical validation.Methods The design concept,technical principles and system composition of the innovative minimally invasive rotary-cutting surgical system for axillary osmidrosis were introduced.A total of 73 patients(146 axillae)with axillary osmidrosis were enrolled as subjects,and underwent surgery using the newly developed surgical system.Clinical validation of the system was performed by evaluating postoperative scarring,odor elimination rate,postoperative complication incidence,and patient satisfaction.Results The study demonstrated favorable clinical outcomes in the following aspects:postoperative scarring,odor elimination rate,postoperative complication incidence,and patient satisfaction.Conclusion The minimally invasive rotary-cutting surgical system for axillary osmidrosis is rationally designed.The rotary-cutting puncture device is safe,effective,minimally invasive,and convenient for axillary osmidrosis surgery,warranting further clinical validation and widespread application.

Objective:To explore the role and mechanism of serum response factor (SRF) and lncRNA FGD5-AS1 in lung adenocarcinoma (LUAD).Methods:The plasma and tissue wax of LUAD patients treated in Tangshan People's Hospital from 2020 to 2022 and the plasma of healthy people were collected. The expression of SRF in LUAD tissues and cells, and the expression of lncRNA FGD5-AS1 in LUAD tissues, plasma and cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The expression levels of SRF and lncRNA FGD5-AS1 in LUAD tissue microarray were detected by immunohistochemistry and in situ hybridization. LUAD cells A549, H1299 and H1975 were cultured in vitro and divided into si-NC and si-SRF groups, si-NC and si-lncRNA FGD5-AS1 groups, pcDNA3.1 and lncRNA FGD5-AS1 groups, si-NC+pcDNA3.1/si-SRF+pcDNA3.1/si-SRF+lncRNA FGD5-AS1 groups. The effects of the above groups on the proliferation, invasion and migration of LUAD cells were detected by CCK-8, cloning formation, EdU, Transwell and scratch test. The JASPAR database was used to predict the downstream lncRNA FGD5-AS1 that can be regulated by SRF; double luciferase experiment, chromatin Immunoprecipitation (CHIP) and electrophoretic mobility shift assay (EMSA) experiment were used to verify the regulatory effect between SRF and lncRNA FGD5-AS1, and the subcutaneous tumorigenesis experiment in nude mice was used to detect the effects of cells that stably knock down SRF and stably overexpress lncRNA FGD5-AS1 on the growth of transplanted tumors. Results:The results of immunohistochemistry showed that the mean optical density of SRF in LUAD tissues (1.49±0.33) was higher than that in adjacent tissues (1.00±0.00, P＜0.001). The expression level of SRF in paraffin tissues of LUAD patients was higher than that in normal tissues adjacent to cancer ( P=0.037). CCK-8, cloning, scratch and Transwell experiments showed that knockdown SRF could inhibit the proliferation, migration and invasion of A549 and H1299 cells, respectively. [For A549 cells: The clone formation count, migration count, invasion count, and 48-h migration distance ratio were (233.70±18.50), (808.70±6.11), (489.70±53.00), and 1.00±0.03, respectively, in the si-NC group; and (131.30±22.50), (403.00±9.54), (372.70±26.27), and 2.14±0.09, respectively, in the si-SRF group. For H1299 cells: The clone formation count, migration count, invasion count, and 48-h migration distance ratio were (194.30±20.98), (988.70±64.52), (907.70±67.02), and 1.00±0.05, respectively, in the si-NC group; and (137.70±7.77), (665.70±157.10), (565.70±67.01), and 1.52±0.03, respectively, in the si-SRF group. All comparisons showed statistically significant differences ( P＜0.05)] JASPAR database prediction shows that SRF and lncRNA FGD5-AS1 have binding site. The double luciferase experiment, CHIP and EMSA experiments showed that SRF could regulate lncRNA FGD5-AS1. In situ hybridization showed that the mean optical density of lncRNA FGD5-AS1 in tissue microarray of LUAD patients (1.28±0.31) was higher than that in adjacent tissues (1.00±0.00, P＜0.001). The results of qRT-PCR experiment showed that the expression level of lncRNA FGD5-AS1 in wax tissues of LUAD patients was higher than that in normal tissues adjacent to cancer ( P=0.017). The expression level of lncRNA FGD5-AS1 in plasma of LUAD patients (3.48±2.62) was higher than that of healthy people (1.02±0.03, P＜0.001). CCK-8, cloning, EDU, scratch and Transwell experiments showed that overexpression of lncRNA FGD5-AS1 could promote cell proliferation [For A549 cells: The clone formation count, EdU-positive cell count, invasion count, and 48-h migration distance ratio were (22.67±5.86), (1.00±0.09), (135.70±13.20), and 0.35±0.02, respectively, in the pcDNA3.1 group; and (46.33±9.07), (1.65±0.10), (205.00±13.23), and 0.20±0.01, respectively, in the FGD5-AS1-overexpressing group. All comparisons showed statistically significant differences ( P＜0.05)], migration and invasion and vice versa [For H1975 cells: The clone formation count, EdU-positive cell count, invasion count, and 48-h migration distance ratio were (75.33±4.16), (1.00±0.02), (258.70±45.79), and 0.18±0.01, respectively, in the NC group; and (37.00±4.00), (0.52±0.07), (130.70±9.07), and 0.53±0.04, respectively, in the lncRNA FGD5-AS1 knockdown group (si-lncRNA FGD5-AS1 group). All comparisons showed statistically significant differences ( P＜0.05)]. Overexpression of lncRNA FGD5-AS1 could rescue the effect of knockdown SRF on the proliferation, migration and invasion of A549 and H1299 cells. The results of subcutaneous tumorigenesis experiment in nude mice indicated that the tumorigenicity of LUAD cells stably knockdown SRF was weakened and vice versa. Conclusion:SRF can promote the progress of LUAD by regulating lncRNA FGD5-AS1.

The medical-industrial fusion training model combines the knowledge and technology of medical and engineering disciplines in the training of oncology graduate students, which can help accurate diagnosis and treatment of tumors, promote cooperation and innovation in oncology research, as well as promote the cultivation and exchanges of composite and innovative medical talents in oncology, promote the innovation and development of oncology diagnostic and treatment technology, and improve the survival rate and quality of life of oncology patients. This paper discusses the application of medical-industrial fusion training model in the training of o ncology professionals, and explores the new teaching mode of medical-industrial fusion thinking in the cultivation of complex and innovative medical talents in oncology under the background of "new medical science".

With the deepening of China's medical reform, people's demand for health is growing, which promotes the construction of "new medicine" and puts forward higher requirements for the cultivation and education of medical students. Undergraduate medical education is a crucial period for the growth of medical students, and how to do a good job in undergraduate teaching under the background of "new medicine" is currently a research hotspot. The clinical teaching stage is an important period for medical students to fully understand clinical disciplines and cultivate their understanding of specialties. Therefore, we should explore new teaching methods and means to adapt to the needs of the new era. In the context of "new medicine", the medical-engineering fusion diagnosis and treatment technology has become an important trend in the clinical diagnosis and treatment of oncology. In order to adapt to this change, clinical teaching and teaching management in oncology also need new exploration and research. Taking the clinical teaching of oncology as an example, this article discusses how to cultivate medical students' thinking of medical-engineering fusion.

Objective:To further explore the role and mechanism of hsa_circ_0001776 and mir-1265 in lung squamous carcinoma by verifying the expression level of hsa_circ_0001776 in plasma, tissues, and cells of lung squamous carcinoma.Methods:Plasma was collected from patients with lung squamous carcinoma treated at Tangshan People's Hospital and healthy individuals from 2020 to 2022. Lung squamous carcinoma tissue microarrays purchased from Shanghai Xinchao Biotechnology Company in 2022. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of hsa_circ_0001776 in lung squamous carcinoma plasma, tissues, and cells, and fluorescence in situ hybridization was used to verify the expression of hsa_circ_0001776 in lung squamous carcinoma. The localization of hsa_circ_0001776 in NCI-H1703 was verified by fluorescence in situ hybridization. The lung squamous carcinoma cells NCI-H1703 and NCI-H226 were cultured in vitro and divided into the circ-negative control (NC) group, hsa_circ_0001776 overexpression group, miR-NC group, miR-1265 mimic group, hsa_circ_0001776+miR-NC group, and hsa_circ_0001776+miR-1265 mimic group.The cell proliferation, motility and apoptosis were detected by the cell counting kit-8 (CCK-8) method, clone formation, Transwell invasion and migration, and scratch assay, and flow cytometry, respectively. The downstream of hsa_circ_0001776 was predicted by circular RNA interactome website, and the interaction between hsa_circ_0001776, miR-1265 was further determined by dual luciferase reporter gene assay, and nude mice subcutaneous tumorigenesis assay detected the growth of transplanted tumors. Results:Fluorescence in situ hybridization results showed that the fluorescence intensity of hsa_circ_0001776 in lung squamous carcinoma tissues was lower than that in paracancerous tissues, and the fluorescence intensity of miR-1265 in lung squamous carcinoma tissues was higher than that in paracancerous tissues (both P＜0.05). The expression level of hsa_circ_0001776 in the plasma of lung squamous carcinoma patients was lower than that in the plasma of healthy people, and the expression level of miR-1265 was higher than that in the plasma of healthy people (both P＜0.05). The expression levels of hsa_circ_0001776 in lung squamous carcinoma cells NCI-H1703, NCI-H226 and SK-MES-1 were lower than that in bronchial epithelial cells BEAS-2B (all P＜0.05), and the relative expression levels of miR-1265 in NCI-H1703 and NCI-H226 were higher than that in human bronchial epithelial cells BEAS -2B (all P＜0.05). The expression of hsa_circ_0001776 was correlated with age, lymph node metastasis, clinical stage, and tumor stage in patients with lung squamous carcinoma (all P＜0.05). Fluorescence in situ hybridization results showed that hsa_circ_0001776 was mainly expressed in the cytoplasm. The results of dual-luciferase reporter assay showed complementary binding of miR-1265 to hsa_circ_0001776. The absorbance values of the hsa_circ_0001776 overexpression group in NCI-H1703 and NCI-H226 cells were lower than that of the circ-NC group ( P＜0.05). The number of cell clones in the hsa_circ_0001776 overexpressed group was (52±3) and (53±4), the number of migrating cells was (476±17) and (113±7), the number of invading cells was (100±2) and (184±2), and the cell migration rate was (25.00±4.36)% and (36.02±5.55)%, which were lower than those of the circ-NC group [(104±4) and (106±2), (783±29) and (517±16), (657±45) and (473±9), (48.95±8.69)% and (48.70±1.57)%, all P＜0.05]. The apoptosis rates in the overexpression hsa_circ_0001776 group were (24.77±2.303)% and (19.67±1.16)%, respectively, both higher than those in the circ-NC group [(11.83±1.15)% and (9.50±0.66)%, respectively, both P＜0.05]. MiR-1265 mimic group had a higher apoptotic rate in the NCI-H1703 and NCI-H226 than those of the miR-NC groups ( P＜0.05). miR-1265 mimic group had (56±13) and (51±8) cell clones, (556±13) and (405±6) migrating cells, (486±6) and (359±7) invading cells, cell migration rates of (68.56±5.51)%, (81.74±8.04)%, were higher than those of miR-NC group [(31±4) and (21±8), (154±19) and (186±5), (227±6) and (176±7), (25.83±4.26)% and (53.12±4.14) %, all P＜0.05]. The apoptotic rates in the miR-1265 mimic group were (11.83±2.55)% and (17.50±1.05)%, respectively, which were lower than those in the miR-NC group [(32.67±4.44)% and (39.90±2.88)%, respectively, both P<0.05]. The absorbance values of NCI-H1703 and NCI-H226 in the overexpression of hsa_circ_0001776+miR-1265 mimic group were higher than those of the overexpression of hsa_circ_0001776+miR-NC group ( P<0.05). The overexpression of hsa_circ_0001776+miR-1265 mimic group had (128±15) and (133±8) cell clones, (623±10) and (310±7) migrating cells, (643±16) and (420±7) invading cells, (66.39±4.46)% cell migration rate and (68.60±3.53)%, were higher than those of the hsa_circ_0001776+miR-NC group [(86±7) and (80±16), (380±11) and (115±5), (152±7) and (94±4), respectively, (31.41±5.91)% and (30.94±0.67)%, all P＜0.05]. The apoptotic rates in the overexpression of hsa_circ_0001776+miR-1265 mimic group were (19.27±0.15)% and (11.53±0.75)%, respectively, both lower than those in the overexpression of hsa_circ_0001776+miR-NC group [(27.77±1.29)% and (18.43±0.71)%, both P＜0.05]. The results of the subcutaneous tumorigenesis assay in nude mice showed that the volume of tumors in the overexpression of hsa_circ_0001776 group was lower than that in the circ-NC group ( P＜0.05). Conclusion:hsa_circ_0001776 is downregulated in lung squamous cell carcinoma, and hsa_circ_0001776 can inhibit the development of lung squamous cell carcinoma by targeting miR-1265.

Background and objective Isoliquiritigenin(ISL)is an important pharmacological constituent of Glycyrrhiza glabra,which possesses a range of physiological and pharmacological activities,as well as significant antitumor ac-tivity,and can be used as a potential drug for targeted cancer therapy.LINC01503 is an oncogene,which has been closely asso-ciated with the malignant biological processes of many cancers.The aim of this study was to investigate the effects of ISL on the proliferation,apoptosis,invasion and migration oflung squamous carcinoma cells by regulating LINC01503.Methods Plasma was collected from lung squamous carcinoma patients and healthy individuals treated at Tangshan People's Hospital from Janu-ary 2021 to December 2022.The expression of LINC01503 in lung squamous carcinoma plasma,tissues and cells was detected by real-time quantitative fluorescence polymerase chain reaction(qRT-PCR).Lung squamous carcinoma cells were treated with different concentrations of ISL for 24 h,and LINC01503 expression was detected by qRT-PCR.The cells were treated in groups:si-NC group,si-LINC01503 group,DMSO(0.1％dimethyl sulfone)group,ISL group,pc DNA3.1(+)-NC group,pc DNA3.1(+)-LINC01503 group,ISL+pc DNA3.1(+)-NC group and ISL+pc DNA3.1(+)-LINC01503 groups.CCK-8 assay,clone formation assay,flow cytometry,Transwell assay and scratch assay were used to explore the effect of LINC01503 on the functional phenotype of lung squamous carcinoma cells.Results Fluorescence in situ hybridization results showed that the average fluorescence intensity of LINC01503 in tissue microarrays of lung squamous carcinoma patients was higher than that in paracancerous tissues(P＜0.05).The expression of LINC01503 in the plasma of patients with lung squamous carcinoma was higher than that in the plasma of healthy individuals(P＜0.05).Knockdown of LINC01503 inhibited the proliferation,invasion and migration of lung squamous carcinoma cells and promoted apoptosis(P＜0.05).ISL inhibited the proliferation,invasion,migration and promoted apoptosis of lung squamous carcinoma cells(P＜0.05).Overexpression of LINC01503 followed by intervention with ISL reversed the promotional effect of overexpression of LINC01503 on the proliferation,invasion and migration of lung squamous carcinoma cells as well as the inhibitory effect on apoptosis(P＜0.05).Conclusion LINC01503 was highly expressed in lung squamous carcinoma,and LINC01503 could promote the proliferation,invasion and migra-tion of lung squamous carcinoma cells and inhibit the apoptosis,ISL could inhibit the proliferation,invasion and migration of lung squamous carcinoma cells and promote apoptosis of lung squamous carcinoma cells by regulating the expression of LINC01503.

Objective:To further explore the role and mechanism of hsa_circ_0001776 and mir-1265 in lung squamous carcinoma by verifying the expression level of hsa_circ_0001776 in plasma, tissues, and cells of lung squamous carcinoma.Methods:Plasma was collected from patients with lung squamous carcinoma treated at Tangshan People's Hospital and healthy individuals from 2020 to 2022. Lung squamous carcinoma tissue microarrays purchased from Shanghai Xinchao Biotechnology Company in 2022. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of hsa_circ_0001776 in lung squamous carcinoma plasma, tissues, and cells, and fluorescence in situ hybridization was used to verify the expression of hsa_circ_0001776 in lung squamous carcinoma. The localization of hsa_circ_0001776 in NCI-H1703 was verified by fluorescence in situ hybridization. The lung squamous carcinoma cells NCI-H1703 and NCI-H226 were cultured in vitro and divided into the circ-negative control (NC) group, hsa_circ_0001776 overexpression group, miR-NC group, miR-1265 mimic group, hsa_circ_0001776+miR-NC group, and hsa_circ_0001776+miR-1265 mimic group.The cell proliferation, motility and apoptosis were detected by the cell counting kit-8 (CCK-8) method, clone formation, Transwell invasion and migration, and scratch assay, and flow cytometry, respectively. The downstream of hsa_circ_0001776 was predicted by circular RNA interactome website, and the interaction between hsa_circ_0001776, miR-1265 was further determined by dual luciferase reporter gene assay, and nude mice subcutaneous tumorigenesis assay detected the growth of transplanted tumors. Results:Fluorescence in situ hybridization results showed that the fluorescence intensity of hsa_circ_0001776 in lung squamous carcinoma tissues was lower than that in paracancerous tissues, and the fluorescence intensity of miR-1265 in lung squamous carcinoma tissues was higher than that in paracancerous tissues (both P＜0.05). The expression level of hsa_circ_0001776 in the plasma of lung squamous carcinoma patients was lower than that in the plasma of healthy people, and the expression level of miR-1265 was higher than that in the plasma of healthy people (both P＜0.05). The expression levels of hsa_circ_0001776 in lung squamous carcinoma cells NCI-H1703, NCI-H226 and SK-MES-1 were lower than that in bronchial epithelial cells BEAS-2B (all P＜0.05), and the relative expression levels of miR-1265 in NCI-H1703 and NCI-H226 were higher than that in human bronchial epithelial cells BEAS -2B (all P＜0.05). The expression of hsa_circ_0001776 was correlated with age, lymph node metastasis, clinical stage, and tumor stage in patients with lung squamous carcinoma (all P＜0.05). Fluorescence in situ hybridization results showed that hsa_circ_0001776 was mainly expressed in the cytoplasm. The results of dual-luciferase reporter assay showed complementary binding of miR-1265 to hsa_circ_0001776. The absorbance values of the hsa_circ_0001776 overexpression group in NCI-H1703 and NCI-H226 cells were lower than that of the circ-NC group ( P＜0.05). The number of cell clones in the hsa_circ_0001776 overexpressed group was (52±3) and (53±4), the number of migrating cells was (476±17) and (113±7), the number of invading cells was (100±2) and (184±2), and the cell migration rate was (25.00±4.36)% and (36.02±5.55)%, which were lower than those of the circ-NC group [(104±4) and (106±2), (783±29) and (517±16), (657±45) and (473±9), (48.95±8.69)% and (48.70±1.57)%, all P＜0.05]. The apoptosis rates in the overexpression hsa_circ_0001776 group were (24.77±2.303)% and (19.67±1.16)%, respectively, both higher than those in the circ-NC group [(11.83±1.15)% and (9.50±0.66)%, respectively, both P＜0.05]. MiR-1265 mimic group had a higher apoptotic rate in the NCI-H1703 and NCI-H226 than those of the miR-NC groups ( P＜0.05). miR-1265 mimic group had (56±13) and (51±8) cell clones, (556±13) and (405±6) migrating cells, (486±6) and (359±7) invading cells, cell migration rates of (68.56±5.51)%, (81.74±8.04)%, were higher than those of miR-NC group [(31±4) and (21±8), (154±19) and (186±5), (227±6) and (176±7), (25.83±4.26)% and (53.12±4.14) %, all P＜0.05]. The apoptotic rates in the miR-1265 mimic group were (11.83±2.55)% and (17.50±1.05)%, respectively, which were lower than those in the miR-NC group [(32.67±4.44)% and (39.90±2.88)%, respectively, both P<0.05]. The absorbance values of NCI-H1703 and NCI-H226 in the overexpression of hsa_circ_0001776+miR-1265 mimic group were higher than those of the overexpression of hsa_circ_0001776+miR-NC group ( P<0.05). The overexpression of hsa_circ_0001776+miR-1265 mimic group had (128±15) and (133±8) cell clones, (623±10) and (310±7) migrating cells, (643±16) and (420±7) invading cells, (66.39±4.46)% cell migration rate and (68.60±3.53)%, were higher than those of the hsa_circ_0001776+miR-NC group [(86±7) and (80±16), (380±11) and (115±5), (152±7) and (94±4), respectively, (31.41±5.91)% and (30.94±0.67)%, all P＜0.05]. The apoptotic rates in the overexpression of hsa_circ_0001776+miR-1265 mimic group were (19.27±0.15)% and (11.53±0.75)%, respectively, both lower than those in the overexpression of hsa_circ_0001776+miR-NC group [(27.77±1.29)% and (18.43±0.71)%, both P＜0.05]. The results of the subcutaneous tumorigenesis assay in nude mice showed that the volume of tumors in the overexpression of hsa_circ_0001776 group was lower than that in the circ-NC group ( P＜0.05). Conclusion:hsa_circ_0001776 is downregulated in lung squamous cell carcinoma, and hsa_circ_0001776 can inhibit the development of lung squamous cell carcinoma by targeting miR-1265.

Objective To compare and analyze clinical effects of three correction methods in type Ⅲnipple retraction.Methods A total of 93 patients with type Ⅲ nipple retraction were retrospectively enrolled at Clifford Hospital between May 2018 and December 2023.Based on the different surgical methods employed,they were categorized into three groups:group A(silk traction method,n=30),group B(areola double-flap method,n=31),and group C(areola single-flap method,n=32).The study compared the operation time,therapeutic efficacy,hemodynamic disorders,improvement in nipple appearance and function,complications,patient satisfac-tion,and recurrence rates among these three groups.Results The operation duration was significantly longer in group B compared to groups A and C(P<0.05).Group C exhibited a significantly higher total response rate than groups A and B(P<0.05),while no significant difference was observed between groups A and B(P>0.05).There were no significant differences in the incidence of hemodynamic disorders among the three groups(P>0.05).The improvement scores for nipple appearance and function were significantly higher in group C compared to groups A and B(P<0.05),with no significant difference between groups A and B(P>0.05).The incidence of complications was lower,satisfaction was higher,both being statistically significant,in group C compared to groups A and B(P<0.05),but there were no significant differences in the incidence of complications or satisfaction between groups A and B(P>0.05).The recurrence rate was significantly lower in group B and group C than in group A(P<0.05).Conclusion The correction effect of the areola single-flap method is superior to that of the silk trac-tion method and areola double-flap method in patients with type Ⅲ nipple retraction,thereby enhancing clinical efficacy,patient satisfaction,nipple aesthetics,and functionality while reducing complications and recurrence rates.