1.Tongue squamous cell carcinoma-targeting Au-HN-1 nanosystem for CT imaging and photothermal therapy.
Ming HAO ; Xingchen LI ; Xinxin ZHANG ; Boqiang TAO ; He SHI ; Jianing WU ; Yuyang LI ; Xiang LI ; Shuangji LI ; Han WU ; Jingcheng XIANG ; Dongxu WANG ; Weiwei LIU ; Guoqing WANG
International Journal of Oral Science 2025;17(1):9-9
Tongue squamous cell carcinoma (TSCC) is a prevalent malignancy that afflicts the head and neck area and presents a high incidence of metastasis and invasion. Accurate diagnosis and effective treatment are essential for enhancing the quality of life and the survival rates of TSCC patients. The current treatment modalities for TSCC frequently suffer from a lack of specificity and efficacy. Nanoparticles with diagnostic and photothermal therapeutic properties may offer a new approach for the targeted therapy of TSCC. However, inadequate accumulation of photosensitizers at the tumor site diminishes the efficacy of photothermal therapy (PTT). This study modified gold nanodots (AuNDs) with the TSCC-targeting peptide HN-1 to improve the selectivity and therapeutic effects of PTT. The Au-HN-1 nanosystem effectively targeted the TSCC cells and was rapidly delivered to the tumor tissues compared to the AuNDs. The enhanced accumulation of photosensitizing agents at tumor sites achieved significant PTT effects in a mouse model of TSCC. Moreover, owing to its stable long-term fluorescence and high X-ray attenuation coefficient, the Au-HN-1 nanosystem can be used for fluorescence and computed tomography imaging of TSCC, rendering it useful for early tumor detection and accurate delineation of surgical margins. In conclusion, Au-HN-1 represents a promising nanomedicine for imaging-based diagnosis and targeted PTT of TSCC.
Tongue Neoplasms/diagnostic imaging*
;
Carcinoma, Squamous Cell/diagnostic imaging*
;
Animals
;
Gold/chemistry*
;
Mice
;
Photothermal Therapy/methods*
;
Tomography, X-Ray Computed
;
Photosensitizing Agents
;
Metal Nanoparticles
;
Humans
;
Cell Line, Tumor
2.Salivary protease spectrum biomarkers of oral cancer.
Yun FENG ; Qian LI ; Jiao CHEN ; Ping YI ; Xin XU ; Yaping FAN ; Bomiao CUI ; Yu YU ; Xiaoying LI ; Yue DU ; Qianming CHEN ; Lingling ZHANG ; Jingjing JIANG ; Xuedong ZHOU ; Ping ZHANG
International Journal of Oral Science 2019;11(1):7-7
Proteases are important molecules that are involved in many physiological and pathological processes of the human body, such as growth, apoptosis and metastasis cancer cells. They are potential targets in cancer diagnosis and biotherapy. In this study, we analyzed the salivary protease spectrum of patients with oral squamous cell carcinoma (OSCC), oral benign masses and chronic periodontitis, as well as that of health, using human protease array kits, enzyme-linked immunosorbent assay, western blot and immunofluorescence. The salivary protease spectrum was found to be associated with oral diseases. For example, the saliva of patients with OSCC contained increased numbers of proteases than those of other oral diseases and health. The levels of matrix metalloproteinase (MMP)-1, MMP-2, MMP-10, MMP-12, A disintegrin and metalloprotease (ADAM)9, A disintegrin and metalloprotease with thrombospondin type 13 motifs (ADAMST13), cathepsin V and kallikrein 5 in the saliva of patients with OSCC were significantly increased compared with those of other groups. Taking MMP-1, cathepsin V, kallikrein 5 and ADAM9 as biomarkers of OSCC, cutoff values were199, 11.34, 9.29 and 202.55 pg·mL, respectively. From the area under the curve, sensitivity and specificity, the combination of cathepsin V/kallikrein5/ADAM9 was an optimal biomarker for diagnosing OSCC. Thus, analysis of the salivary protease spectrum may be an innovative and cost-efficient approach to evaluating the health status of the oral cavity. Specifically, increases in cathepsin V, kallikrein 5 and ADAM9 may be useful biomarkers in the screening and diagnosis of OSCC.
ADAM Proteins
;
Biomarkers, Tumor
;
analysis
;
Carcinoma, Squamous Cell
;
diagnosis
;
metabolism
;
Humans
;
Matrix Metalloproteinase 9
;
analysis
;
Membrane Proteins
;
Mouth Neoplasms
;
diagnosis
;
metabolism
;
Saliva
;
chemistry
3.Effect of DJ-1 silencing by RNA interference on growth of xenografted human laryngeal squamous cell carcinoma Hep-2 cells in nude mice.
Zhisen SHEN ; Hongxia DENG ; Dong YE ; Jian ZHANG ; Shijie QIU ; Qun LI ; Xiang CUI
Journal of Zhejiang University. Medical sciences 2016;45(4):349-355
To investigate the effect of silencing DJ-1 on xenografted human laryngeal squamous cell carcinoma (LSCC) Hep-2 cells in nude mice.Xenograft model of human LSCC was established by subcutaneous transplantation of Hep-2 cells in 24 nude mice. The LSCC-bearing nude mice were randomly divided into 3 groups (=8 in each):DJ-1 siRNA low dose group and DJ-1 siRNA high dose group were injected in tumors with 20 μg of DJ-1 siRNA or 40 μg of DJ-1 siRNA in 50 μL, respectively; control group was injected with 5% glucose solution in 50 μL, twice a week for 3 weeks. The weight and size of tumors were measured before injection. The animals were sacrificed 48 h after the final treatment, and the tumors were harvested and weighed. The apoptosis and proliferation of tumor cells were determined; the expressions of Caspase-3 and Ki-67 in tumor specimens were detected with immunohistochemistry. The expression of DJ-1, PTEN, survivin mRNA and protein in tumor tissues were detected by RT-PCR and Western blotting, respectively.Tumor weight in low dose group[(0.66±0.15)g] and high dose group[(0.48±0.11)g] were significantly lower than that in control group[(0.83±0.16)g, all<0.05]. The inhibition rates of low dose group and high dose group were (20.48±0.18)% and (42.16±0.13)%, respectively. Immunohistochemistry showed that the expression of Caspase-3 was increased and Ki-67 was reduced in tumor specimens, compared with the control group (all<0.05). RT-PCR and Western blot results showed that in low dose group and high dose group the mRNA and protein expression of DJ-1 and survivin significantly decreased (all<0.05), while PTEN mRNA and protein content increased (all<0.05).High dose DJ-1 siRNA can inhibit the tumor growth in human LSCC xenograft nude mouse model, which indicates that down-regulating DJ-1 and survivin, and up-regulating PTEN expression may lead to blockage of PI3K-PKB/Akt signaling pathway and promoting tumor cell apoptosis.
Animals
;
Antineoplastic Agents
;
pharmacology
;
Apoptosis
;
drug effects
;
genetics
;
Carcinoma, Squamous Cell
;
chemistry
;
genetics
;
physiopathology
;
Caspase 3
;
analysis
;
drug effects
;
Cell Line, Tumor
;
chemistry
;
drug effects
;
physiology
;
transplantation
;
Cell Proliferation
;
drug effects
;
Down-Regulation
;
Gene Expression Regulation
;
drug effects
;
genetics
;
physiology
;
Head and Neck Neoplasms
;
chemistry
;
genetics
;
physiopathology
;
Heterografts
;
drug effects
;
physiology
;
Humans
;
Inhibitor of Apoptosis Proteins
;
analysis
;
drug effects
;
Ki-67 Antigen
;
analysis
;
drug effects
;
Laryngeal Neoplasms
;
chemistry
;
genetics
;
physiopathology
;
Mice, Nude
;
PTEN Phosphohydrolase
;
analysis
;
drug effects
;
Phosphatidylinositol 3-Kinases
;
drug effects
;
Protein Deglycase DJ-1
;
pharmacology
;
Proto-Oncogene Proteins c-akt
;
drug effects
;
RNA Interference
;
physiology
;
RNA, Messenger
;
pharmacology
;
RNA, Small Interfering
;
physiology
;
Signal Transduction
;
drug effects
;
genetics
;
physiology
4.PRKAR1α expression in non-small cell lung cancer and its clinicopathologic significance.
Shaoqiang WANG ; Yuanda CHENG ; Zhiwei HE ; Wolong ZHOU ; Yang GAO ; Chaojun DUAN ; Chunfang ZHANG
Journal of Central South University(Medical Sciences) 2016;41(11):1148-1154
To evaluate the expression of cAMP-dependent protein kinase type I-alpha regulatory subunit (PRKAR1α) in non-small cell lung cancer (NSCLC) and its correlation with clinicopathological features.
Methods: PRKAR1α expressions in 79 NSCLC patients and matched adjacent non-carcinoma tissues were analyzed by using qRT-PCR and immunohistochemistry.
Results: The negative rates of PRKAR1α protein in NSCLC, lung squamous cell carcinoma (SCL) and lung adenocarcinoma (ACL) were 58.2%, 77.8%, 32.4%, respectively. Compared to the matched adjacent non-carcinoma tissues, there were significant differences in levels of PRKAR1α mRNA and protein in ACL (P<0.05), but not in SCL and overall NSCLC (P>0.05). The expression of PRKAR1α protein was positively correlated with histological type, TNM stage, and lymph node metastasis (P<0.05). Tumor size and histogenesis differentiation were not related to the decreased PRKAR1α (P>0.05).
Conclusion: Low expression of PRKAR1α in ACL might be involved in the pathogenesis, which might serve as a novel diagnostic candidate.
Adenocarcinoma
;
chemistry
;
classification
;
genetics
;
Adenocarcinoma of Lung
;
Biomarkers, Tumor
;
Carcinoma, Non-Small-Cell Lung
;
chemistry
;
genetics
;
Carcinoma, Squamous Cell
;
chemistry
;
genetics
;
Cyclic AMP-Dependent Protein Kinase RIalpha Subunit
;
physiology
;
Female
;
Gene Expression Profiling
;
Humans
;
Immunohistochemistry
;
Lung Neoplasms
;
chemistry
;
classification
;
genetics
;
Lymphatic Metastasis
;
genetics
;
Male
;
Neoplasm Staging
;
RNA, Messenger
5.Clinicopathologic observation of adenoid cystic carcinoma of esophagus.
Yan DU ; Hua ZHAO ; Zhihong ZHANG ; Qinhe FAN ; Guoxin SONG ; Weiming ZHANG ; Cong WANG
Chinese Journal of Pathology 2015;44(1):27-31
OBJECTIVETo study the clinicopathologic features and differential diagnosis of adenoid cystic carcinoma in the esophagus.
METHODSTen cases of primary adenoid cystic carcinoma of the esophagus were retrieved from the archival file. The clinicopathologic and immunohistochemical features were studied. The differential diagnosis was analyzed.
RESULTSThe male-to-female ratio was 9: 1. The age of patients ranged from 59 to 76 years. There were 4 cases with tumor located in mid esophagus, 4 cases with tumor located in mid to lower esophagus and the remaining 2 cases in lower esophagus. Low-power histologic examination showed mainly expansive growth pattern, with cribriform, solid and focal tubular architectures identified. The tumor cells showed nuclear hyperchromasia. Both ductal and myoepithelial differentiation was demonstrated. The stroma showed myxoid degeneration in areas. Comedo-type necrosis was observed in 8 cases and moderate to severe squamous dysplasia was present in one case. Three cases showed focal areas of squamous cell carcinoma. Immunohistochemical study showed that the tumor cells were positive for p63 (10/10), CD117 (10/10) and S-100 protein (9/10). There was focal staining for calponin (2/10) and smooth muscle actin (2/10). The ductal structures expressed CK7 (10/10).
CONCLUSIONSAdenoid cystic carcinoma of the esophagus demonstrates unique morphologic features with expression of S-100 protein and consistent expression of CD117. The above characteristics help to distinguish this entity from basaloid squamous cell carcinoma, mucoepidermoid carcinoma and small cell carcinoma of the esophagus.
Aged ; Calcium-Binding Proteins ; analysis ; Carcinoma, Adenoid Cystic ; chemistry ; pathology ; Carcinoma, Small Cell ; chemistry ; pathology ; Carcinoma, Squamous Cell ; chemistry ; pathology ; Esophageal Neoplasms ; chemistry ; pathology ; Female ; Humans ; Immunohistochemistry ; Male ; Microfilament Proteins ; analysis ; Middle Aged ; S100 Proteins ; analysis
6.Effect of nano-realgar on proliferation and apoptosis of human cervical carcinoma cells.
Lijie LI ; Luying WANG ; Songshu XIAO ; Yueran LI ; Chunxia CHENG ; Min XUE
Journal of Central South University(Medical Sciences) 2015;40(10):1068-1075
OBJECTIVE:
To investigate the effect of nano-realgar on proliferation and apoptosis of cervical cancer cells.
METHODS:
Different cervical cancer cell lines (Caski/HPV16+, adeno carcinoma; Hela/HPV18+, squmous carcinoma; C33A/HPV-, adeno carcinoma) were incubated with nano-realgar at different concentrations (5, 10, 20, 40 mg/L) for different times (24, 48, 72, 96 h). The morphology was observed under phase contrast microscope. The cell viability and apoptosis were examined by MTT and flow cytometry, respectively.
RESULTS:
The inhibitory effect of nano-realgar on the proliferation of cervical cancer cells was in a dose-dependent manner, with a range of inhibitory rate from 9.02% to 49.06%. Taking the group (20 mg/L) for an example, the inhibitory rates for Caski, Hela and C33A were 39.15%, 36.17% and 30.56%, respectively. The results of flow cytometry showed that the nano-realgar induced apoptosis in a concentration-dependent manner, with a range of apoptosis rate from 19.29% to 99.54%. Also taking the group (20 mg/L) for an example, the apoptosis rates for Caski, Hela and C33A were (60.43 ± 2.88)%, (41.95 ± 3.01)% and (43.49 ± 2.19)%, respectively. High concentration of nano-realgar (20 or 40 mg/L) could induce block of Hela and Caski at G2/M stage.
CONCLUSION
Nano-realgar can inhibit the proliferation of different cervical carcinoma cell lines and can induce the cell apoptosis. The inhibitory effect on cell proliferation is strongest for Caski, followed by Hela and C33A. It can also induce G2/M stage block on HPV positive cervical cancer cells at high enough concentration.
Adenocarcinoma
;
pathology
;
Apoptosis
;
drug effects
;
Arsenicals
;
chemistry
;
Carcinoma, Squamous Cell
;
pathology
;
Cell Line, Tumor
;
drug effects
;
Cell Proliferation
;
drug effects
;
Female
;
HeLa Cells
;
drug effects
;
Humans
;
Nanoparticles
;
chemistry
;
Sulfides
;
chemistry
;
Uterine Cervical Neoplasms
;
pathology
7.Pseudoepitheliomatous Hyperplasia Mimicking Esophageal Squamous Cell Carcinoma in a Patient with Lye-induced Esophageal Stricture.
Jang Soo HAN ; Sang Woo LEE ; Kang Heum SUH ; Seung Young KIM ; Jong Jin HYUN ; Sung Woo JUNG ; Ja Seol KOO ; Hyung Joon YIM
The Korean Journal of Gastroenterology 2014;63(6):366-368
Pseudoepitheliomatous hyperplasia is a benign condition that may be caused by prolonged inflammation, chronic infection, and/or neoplastic conditions of the mucous membranes or skin. Due to its histological resemblance to well-differentiated squamous cell carcinoma, pseudoepitheliomatous hyperplasia may occasionally be misdiagnosed as squamous cell carcinoma. The importance of pseudoepitheliomatous hyperplasia is that it is a self-limited condition that must be distinguished from squamous cell carcinoma before invasive treatment. We report here on a rare case of esophageal pseudoepitheliomatous hyperplasia in a 67-year-old Korean woman with a lye-induced esophageal stricture. Although esophageal pseudoepitheliomatous hyperplasia is infrequently encountered, pseudoepitheliomatous hyperplasia should be considered in the differential diagnosis of esophageal lesions.
Aged
;
Carcinoma, Squamous Cell/diagnosis
;
Diagnosis, Differential
;
Esophageal Neoplasms/diagnosis
;
Esophageal Stenosis/chemically induced/*diagnosis
;
Esophagoscopy
;
Female
;
Humans
;
Hyperplasia/*diagnosis/pathology
;
Iodides/chemistry
;
Lye/*toxicity
8.Pseudoepitheliomatous Hyperplasia Mimicking Esophageal Squamous Cell Carcinoma in a Patient with Lye-induced Esophageal Stricture.
Jang Soo HAN ; Sang Woo LEE ; Kang Heum SUH ; Seung Young KIM ; Jong Jin HYUN ; Sung Woo JUNG ; Ja Seol KOO ; Hyung Joon YIM
The Korean Journal of Gastroenterology 2014;63(6):366-368
Pseudoepitheliomatous hyperplasia is a benign condition that may be caused by prolonged inflammation, chronic infection, and/or neoplastic conditions of the mucous membranes or skin. Due to its histological resemblance to well-differentiated squamous cell carcinoma, pseudoepitheliomatous hyperplasia may occasionally be misdiagnosed as squamous cell carcinoma. The importance of pseudoepitheliomatous hyperplasia is that it is a self-limited condition that must be distinguished from squamous cell carcinoma before invasive treatment. We report here on a rare case of esophageal pseudoepitheliomatous hyperplasia in a 67-year-old Korean woman with a lye-induced esophageal stricture. Although esophageal pseudoepitheliomatous hyperplasia is infrequently encountered, pseudoepitheliomatous hyperplasia should be considered in the differential diagnosis of esophageal lesions.
Aged
;
Carcinoma, Squamous Cell/diagnosis
;
Diagnosis, Differential
;
Esophageal Neoplasms/diagnosis
;
Esophageal Stenosis/chemically induced/*diagnosis
;
Esophagoscopy
;
Female
;
Humans
;
Hyperplasia/*diagnosis/pathology
;
Iodides/chemistry
;
Lye/*toxicity
9.Huge clear cell squamous cell carcinoma of the head.
Chinese Medical Journal 2013;126(14):2646-2646
10.Expression of connexin 43 in tongue carcinogenesis.
Yan FENG ; Xiao-jie KANG ; Chun-hui LI ; Min-hai NIE
Chinese Journal of Medical Genetics 2013;30(2):237-239
OBJECTIVETo study the expression of connexin 43 (Cx43) in various stages of oral carcinogenesis and explore the relation between Cx43 and oral mucous carcinogenesis.
METHODS4-nitroquinoline-1-oxide (4NQO) was used for inducing oral carcinogenesis in SD rats. Tissue samples were obtained from various stages of the disease including normal oral mucosa, precancerous lesions and oral squamous cell carcinoma. Immunohistochemical method was used to determine the expression of Cx43 in various stages of oral carcinogenesis.
RESULTSIn the normal rat lingual mucosa, immunohistochemical staining of Cx43 protein was mainly found in the cell membrane, weakly positive in the basal cell layer, increased in stratum spinosum and stratum granulosum, but was negative in the stratum corneum of normal epithelia. Compared with normal epithelia, was significantly decreased in dysplastic and cancerous oral epithelia the staining. The positive rates of Cx43 were respectively 100.00% (10/10), 85.71% (12/14), 66.67% (8/12), 40.00% (4/10), and 33.33% (4/12) in tongue carcinogenesis (in normal, mild, moderate and severe dysplasia, and squamous cell carcinoma tissues). The differences were statistically significant (P<0.05).
CONCLUSIONExpression level of Cx43 protein was dramatically decreased with the development of rat tongue carcinoma induced by 4NQO, suggesting that abnormal expression of Cx43 protein is involved in oral mucosa carcinogenesis. Decreased Cx43 expression is an early sign of oral mucosa carcinogenesis.
4-Nitroquinoline-1-oxide ; toxicity ; Animals ; Carcinoma, Squamous Cell ; chemically induced ; chemistry ; etiology ; Connexin 43 ; analysis ; genetics ; physiology ; Male ; Rats ; Rats, Sprague-Dawley ; Tongue Neoplasms ; chemically induced ; chemistry ; etiology

Result Analysis
Print
Save
E-mail