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13 results on '"Qiao, Xiaowen"'

12. HPV E7-mediated NCAPH ectopic expression regulates the carcinogenesis of cervical carcinoma via PI3K/AKT/SGK pathway

Author

Xiujie Cui, Liang Liu, Jiaxiang Lin, Wei Pan, John D. Hayball, Ranran Zhang, Tamara H. Cooper, Ying Zou, Xiaowen Qiao, Meng Wang, Xiao Wang, Shule Zhang, Yabin Zhou, Wang, Meng, Qiao, Xiaowen, Cooper, Tamara, Pan, Wei, Liu, Liang, Hayball, John, Lin, Jiaxiang, Cui, Xiujie, Zhou, Yabin, Zhang, Shule, Zou, Ying, Zhang, Ranran, and Wang, Xiao

Subjects
Cancer Research, cervical cancer, Carcinogenesis, Papillomavirus E7 Proteins, Uterine Cervical Neoplasms, Cell Cycle Proteins, medicine.disease_cause, Ectopic Gene Expression, Phosphatidylinositol 3-Kinases, Cell Movement, E2F1, Promoter Regions, Genetic, Tumor Stem Cell Assay, Cervical cancer, lcsh:Cytology, Nuclear Proteins, Prognosis, Gene Expression Regulation, Neoplastic, Treatment Outcome, Female, Protein Binding, Signal Transduction, Adult, Epithelial-Mesenchymal Transition, Immunology, Mice, Nude, Biology, Protein Serine-Threonine Kinases, Models, Biological, Article, Immediate-Early Proteins, Cellular and Molecular Neuroscience, Medical research, Cell Line, Tumor, medicine, Gene silencing, Animals, Humans, Neoplasm Invasiveness, lcsh:QH573-671, PI3K/AKT/mTOR pathway, Cell Proliferation, gynecological tumors, tumor size, NCAPH-induced cell proliferation, Cell Biology, medicine.disease, Condensin I complex, Transcription Factor AP-1, Cancer cell, Cancer research, Ectopic expression, Protein Multimerization, Proto-Oncogene Proteins c-akt, E2F1 Transcription Factor
Abstract

Cervical cancer is one of the most common gynecological tumors in the world, and human papillomavirus (HPV) infection is its causative agent. However, the molecular mechanisms involved in the carcinogenesis of cervical cancer still require clarification. Here we found that knockdown of Non-SMC (Structural Maintenance of Chromosomes) condensin I complex subunit H (NCAPH) gene expression significantly inhibited the proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) of cervical cancer cells in vitro, and restrained xenograft tumor formation in vivo. Intriguingly, HPV E7 could form a positive feedback loop with NCAPH. E7 upregulated NCAPH gene expression via E2F1 which initiated NCAPH transcription by binding to its promoter directly. Silencing of NCAPH reduced E7 transcription via promoting the transition of AP-1 heterodimer from c-Fos/c-Jun to Fra-1/c-Jun. Moreover, the E7-mediated NCAPH overexpression was involved in the activation of the PI3K/AKT/SGK signaling pathway. In vivo, NCAPH expression in cervical cancer tissues was significantly higher than which in normal cervix and high-grade squamous intraepithelial lesion (HSIL) tissues, and its expression was significantly correlated with tumor size, depth of invasion and lymph node metastasis. Patients with high NCAPH expression had a significantly better survival outcomes than those with low-expression, suggesting that NCAPH-induced cell proliferation might sensitize cancer cells to adjuvant therapy. In conclusion, our results revealed the role of NCAPH in the carcinogenesis of cervical cancer in vitro and in vivo. The interaction between E7 and NCAPH expands the mechanism of HPV induced tumorigenesis and that of host genes regulating HPV E7.

Published
2020

13. WFDC3 sensitizes colorectal cancer to chemotherapy by regulating ATM/ATR kinase signaling pathway.

Author

Yang X, Weng K, Xing P, Chen J, Hao H, Liu T, Song T, Qiao X, Hou Y, Chen J, Ran Y, Song L, Chen B, Yang H, Wang Z, Di J, Jiang B, and Su X

Subjects
Humans, Mice, Animals, Mice, Nude, Cell Line, Tumor, Antineoplastic Agents pharmacology, Female, Mice, Inbred BALB C, Male, DNA Damage, Gene Expression Regulation, Neoplastic drug effects, Xenograft Model Antitumor Assays, Colorectal Neoplasms drug therapy, Colorectal Neoplasms metabolism, Colorectal Neoplasms pathology, Colorectal Neoplasms genetics, Ataxia Telangiectasia Mutated Proteins metabolism, Ataxia Telangiectasia Mutated Proteins genetics, Oxaliplatin pharmacology, Signal Transduction drug effects, Drug Resistance, Neoplasm
Abstract

Chemoresistance is an ongoing challenge for colorectal cancer (CRC) that significantly compromises the anti-tumor efficacy of current drugs. Identifying effective targets or drugs for overcoming chemoresistance is urgently needed. Our previous study showed that WFDC3 served as a tumor suppressor that hindered CRC metastasis. However, the function of WFDC3 in chemotherapy remains unknown. Here, we found that high WFDC3 expression in CRC patients treated with oxaliplatin was associated with a better prognosis. Concordantly, overexpression of WFDC3 significantly increased sensitivity to oxaliplatin in CRC cells, whereas knocking down WFDC3 led to oxaliplatin resistance. In addition, WFDC3 promoted oxaliplatin-mediated suppression of tumor growth in vivo. Subsequently, we found that WFDC3 could enhance oxaliplatin-induced DNA damage through inhibiting ATM/ATR signaling. WFDC3 knockdown showed the opposite effects. Moreover, a combination treatment of oxaliplatin and inhibitors for ATM or ATR partially reversed chemoresistance to oxaliplatin in CRC cells with low WFDC3 expression. Our results demonstrate that WFDC3 is possibly a biomarker for increasing oxaliplatin sensitivity in CRC by modulating ATM/ATR kinase signaling. Thus, a combination of oxaliplatin with an ATM or ATR inhibitor is a potential treatment option for improving CRC outcome., (© 2025 Federation of American Societies for Experimental Biology.)

Published
2025
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