Objective To investigate the functions of FABP5 in the carcinogenesis and development of cervical cancer. Methods The expression of FABP5 was detected in several cervical cancer cell lines (C33A, Siha, Caski, HeLa and HCC94), 206 cases of cervical cancer tissues with stageⅠa2?Ⅱa2 and 40 cases of normal cervical tissues by real?time PCR and Western blotting. Then, the cells were infected with lentivirus?mediated siRNA?targeting FABP5. CCK?8 cell proliferation, colony formation, wound healing and transwell assays were used to investigate the effects of FABP5 on in vitro cell proliferation, migration and invasion. And in vivo xenograft model and lung metastasis model were used to observe the transplanted tumor growth and metastasis in female athymic nude mice. Furthermore, the total protein and RNA were extracted from the primary xenografts to determine the expression levels of FABP5, metalloproteinase?2 and metalloproteinase?9 using Enzyme linked immunosorbent assay ( ELISA ), real?time PCR and Western blotting.Results FABP5 expression was found to be significantly unregulated in cervical cancer tissues than that in normal cervical tissues ( P＜0.05). Compared with the Siha?NC group and uninfected group, the expression of FABP5 mRNA and protein in Siha?FABP5?RNAi group was significantly inhibited along with the decrease of cell proliferation, colony formation, wound healing and invasion ability. The clone formation rates of Siha cells in uninfected group, Siha?NC group and Siha?FABP5?RNAi group were (84.6± 4.5)%, (84.6±5.1)% and (21.2±2.6)%, respectively. Moreover, the transwell assay showed that invasive cells in three groups were (72.8±4.7)／HPF, (72.6± 3.3)／HPF and ( 21.4± 2.3)／HPF, respectively. All of the difference was statistically significant (P＜0.05). Furthermore, FABP5 silencing significantly reduced tumor growth and lung metastases in nude mice in vivo ( P＜0.001). The subcutaneously xenografted volume in uninfected group, Siha?NC group and Siha?FABP5?RNAi group was (921.4±63.0) mm3, (1 021.4±56.0) mm3 and (139.6±36.0) mm3, respectively. The real?time quantitative PCR results showed that the relative expression levels of MMP?2 and MMP?9 mRNA were 1.00±0.10 and 1.00±0.10, 1.00±0.10 and 1.00±0.10 as well as 0.34±0.13 and 0.38±0.17 in xenografted tumor tissues of uninfected group, Siha?NC group and Siha?FABP5?RNAi group, respectively. MMP?2 and MMP?9 was significantly downregulated after FABP5 inhibition(P＜0.05). Additionally, the protein expression trend of MMP?2 and MMP?9 in three groups was consistent with the mRNA levels. Conclusion FABP5 might promote the carcinogenesis and metastasis of cervical cancer via up?regulating MMP?2 and MMP?9.

Objective To investigate the functions of FABP5 in the carcinogenesis and development of cervical cancer. Methods The expression of FABP5 was detected in several cervical cancer cell lines (C33A, Siha, Caski, HeLa and HCC94), 206 cases of cervical cancer tissues with stageⅠa2?Ⅱa2 and 40 cases of normal cervical tissues by real?time PCR and Western blotting. Then, the cells were infected with lentivirus?mediated siRNA?targeting FABP5. CCK?8 cell proliferation, colony formation, wound healing and transwell assays were used to investigate the effects of FABP5 on in vitro cell proliferation, migration and invasion. And in vivo xenograft model and lung metastasis model were used to observe the transplanted tumor growth and metastasis in female athymic nude mice. Furthermore, the total protein and RNA were extracted from the primary xenografts to determine the expression levels of FABP5, metalloproteinase?2 and metalloproteinase?9 using Enzyme linked immunosorbent assay ( ELISA ), real?time PCR and Western blotting.Results FABP5 expression was found to be significantly unregulated in cervical cancer tissues than that in normal cervical tissues ( P＜0.05). Compared with the Siha?NC group and uninfected group, the expression of FABP5 mRNA and protein in Siha?FABP5?RNAi group was significantly inhibited along with the decrease of cell proliferation, colony formation, wound healing and invasion ability. The clone formation rates of Siha cells in uninfected group, Siha?NC group and Siha?FABP5?RNAi group were (84.6± 4.5)%, (84.6±5.1)% and (21.2±2.6)%, respectively. Moreover, the transwell assay showed that invasive cells in three groups were (72.8±4.7)／HPF, (72.6± 3.3)／HPF and ( 21.4± 2.3)／HPF, respectively. All of the difference was statistically significant (P＜0.05). Furthermore, FABP5 silencing significantly reduced tumor growth and lung metastases in nude mice in vivo ( P＜0.001). The subcutaneously xenografted volume in uninfected group, Siha?NC group and Siha?FABP5?RNAi group was (921.4±63.0) mm3, (1 021.4±56.0) mm3 and (139.6±36.0) mm3, respectively. The real?time quantitative PCR results showed that the relative expression levels of MMP?2 and MMP?9 mRNA were 1.00±0.10 and 1.00±0.10, 1.00±0.10 and 1.00±0.10 as well as 0.34±0.13 and 0.38±0.17 in xenografted tumor tissues of uninfected group, Siha?NC group and Siha?FABP5?RNAi group, respectively. MMP?2 and MMP?9 was significantly downregulated after FABP5 inhibition(P＜0.05). Additionally, the protein expression trend of MMP?2 and MMP?9 in three groups was consistent with the mRNA levels. Conclusion FABP5 might promote the carcinogenesis and metastasis of cervical cancer via up?regulating MMP?2 and MMP?9.

Objective: To investigate the functions of FABP5 in the carcinogenesis and development of cervical cancer. Methods: The expression of FABP5 was detected in several cervical cancer cell lines (C33A, Siha, Caski, HeLa and HCC94), 206 cases of cervical cancer tissues with stage Ⅰa2-Ⅱa2 and 40 cases of normal cervical tissues by real-time PCR and Western blotting. Then, the cells were infected with lentivirus-mediated siRNA-targeting FABP5. CCK-8 cell proliferation, colony formation, wound healing and transwell assays were used to investigate the effects of FABP5 on in vitro cell proliferation, migration and invasion. And in vivo xenograft model and lung metastasis model were used to observe the transplanted tumor growth and metastasis in female athymic nude mice. Furthermore, the total protein and RNA were extracted from the primary xenografts to determine the expression levels of FABP5, metalloproteinase-2 and metalloproteinase-9 using Enzyme linked immunosorbent assay (ELISA), real-time PCR and Western blotting. Results: FABP5 expression was found to be significantly unregulated in cervical cancer tissues than that in normal cervical tissues (P<0.05). Compared with the Siha-NC group and uninfected group, the expression of FABP5 mRNA and protein in Siha-FABP5-RNAi group was significantly inhibited along with the decrease of cell proliferation, colony formation, wound healing and invasion ability. The clone formation rates of Siha cells in uninfected group, Siha-NC group and Siha-FABP5-RNAi group were (84.6±4.5)%, (84.6±5.1)% and (21.2±2.6)%, respectively. Moreover, the transwell assay showed that invasive cells in three groups were (72.8±4.7)/HPF, (72.6±3.3)/HPF and (21.4±2.3)/HPF, respectively. All of the difference was statistically significant (P<0.05). Furthermore, FABP5 silencing significantly reduced tumor growth and lung metastases in nude mice in vivo (P<0.001). The subcutaneously xenografted volume in uninfected group, Siha-NC group and Siha-FABP5-RNAi group was (921.4±63.0) mm^3, (1 021.4±56.0) mm³ and (139.6±36.0) mm^3, respectively. The real-time quantitative PCR results showed that the relative expression levels of MMP-2 and MMP-9 mRNA were 1.00±0.10 and 1.00±0.10, 1.00±0.10 and 1.00±0.10 as well as 0.34±0.13 and 0.38±0.17 in xenografted tumor tissues of uninfected group, Siha-NC group and Siha-FABP5-RNAi group, respectively. MMP-2 and MMP-9 was significantly downregulated after FABP5 inhibition(P<0.05). Additionally, the protein expression trend of MMP-2 and MMP-9 in three groups was consistent with the mRNA levels. Conclusion FABP5 might promote the carcinogenesis and metastasis of cervical cancer via up-regulating MMP-2 and MMP-9.

OBJECTIVE To investigate the independent risk factors for carbapenem-resistant Klebsiella pneumoniae （CRKP） infection， develop a nomogram prediction model and validate it. METHODS Clinical data of hospitalized patients infected with CRKP between April 2020 and May 2023 at Kunming First People’s Hospital were retrospectively collected and matched 1∶1 with patients infected with carbapenem-susceptible Klebsiella pneumoniae （CSKP） during the same period as the modeling group. Using the same criteria， data from patients hospitalized and infected with CRKP and matched CSKP between June 2023 and June 2024 were collected as the validation group. Univariate analysis， LASSO regression and multivariate Logistic regression were conducted to identify independent risk factors for CRKP infection and to develop a nomogram prediction model. Internal validation of the model was performed using Bootstrap resampling， and external validation was carried out using the data of validation group. The predictive performance of the model was evaluated using receiver operating characteristic （ROC） curves and calibration plots. RESULTS A total of 530 patients were enrolled， with 372 in the modeling group and 158 in the validation group. Cerebrovascular disease， indwelling gastric tube， mechanical ventilation， exposure to carbapenem antibiotics， and exposure to β-lactamase inhibitor compound agents were identified as independent risk factors for CRKP infection （P＜0.05）. The nomogram predicting CRKP infection risk achieved an area under ROC of 0.729 and 0.803 in internal and external validations， respectively. Calibration curves indicated a high degree of consistency between predicted and observed probabilities. CONCLUSIONS Cerebrovascular disease， indwelling gastric tube， mechanical ventilation， exposure to carbapenem antibiotics， and exposure to β-lactamase inhibitor compound agent are independent risk factors for CRKP infection. The developed nomogram model for predicting CRKP infection risk demonstrates good predictive performance and can aid in the early identification of patients at high risk for CRKP infection.