Investigator

Yanping Zhao

Xinjiang Medical University

YZYanping Zhao
Papers(2)
p16 expression and it…FOXM1 Promotes Drug R…
Collaborators(8)
Youxiang HouZhanfei DongZuowei ZouGulina KuerbanHe HuangLe ChongLuhua XiaXinhua Wang
Institutions(4)
Xinjiang Medical Univ…Chinese Academy Of Me…State Key Laboratory …Tumor Hospital Of Gua…

Papers

p16 expression and its correlation with the clinical pathological characteristics of patients with cervical cancer: a systematic review and meta-analysis

Objectives Overexpression of p16 has been documented in a variety of human tumours. Nonetheless, the association between p16 overexpression and the clinicopathological characteristics of patients with cervical cancer remains a subject of debate. This meta-analysis sought to systematically assess the relationship between p16 expression and the clinicopathological features of patients with cervical cancer. Design Systematic review and meta-analysis. Data sources The PubMed, Embase, Cochrane Library (Central), Web of Science (SCI Expanded), and Chinese databases (CNKI, VIP, Wanfang and CBM) were searched through 1 March 2024. Eligibility criteria for selecting studies Case‒control studies examining the association between p16 expression and cervical cancer were analysed to evaluate whether p16 expression was correlated with the clinicopathological characteristics of patients with cervical cancer. Data extraction and synthesis Two independent reviewers employed standardised methods to search, screen and code the included studies. The risk of bias was evaluated using the Cochrane Collaboration tools and the Newcastle-Ottawa Scale. Statistical analyses and data processing were conducted using Review Manager V.5.4, which included heterogeneity tests and sensitivity analyses. Additionally, STATA V.16.0 was used for further sensitivity analyses of the included studies, and publication bias was assessed using Begg’s test. Conclusions The p16 protein is strongly associated with the onset and progression of cervical cancer and serves as a valuable biomarker for its early detection and diagnosis. PROSPERO registration number CRD42024546241.

FOXM1 Promotes Drug Resistance in Cervical Cancer Cells by Regulating ABCC5 Gene Transcription

Objective. The aim of the present study was to investigate the effect of forkhead box M1 (FOXM1) to paclitaxel resistance in cervical cancer cells, to determine the underlying mechanism, and to identify novel targets for the treatment of paclitaxel‐resistant cervical cancer. Methods. Paclitaxel‐resistant Caski cells (Caski/Taxol cells) were established by intermittently exposing the Caski cells to gradually increasing concentrations of paclitaxel. The association between FOXM1, ATP‐binding cassette subfamily C member 5 (ABCC5), and cervical cancer cell drug resistance was assessed by overexpressing or knocking down the expression of FOXM1 in Caski or Caski/Taxol cells. The protein and mRNA expression levels, the ratio of cellular apoptosis, and cell migration as well as intracellular drug concentrations were measured in cells following the different treatments. Results. After the successful establishment of resistant Caski/Taxol cells, cell cycle distribution analysis showed that a significantly larger percentage of Caski/Taxol cells was in the G0/G1 stage compared with the Caski cells (P < 0.01), whereas a significantly larger percentage of Caski cells was in the S and G2/M stage compared with the Caski/Taxol cells following treatment with paclitaxel (P < 0.01). Both the protein and mRNA expression levels of FOXM1 and ABCC5 transporters were significantly higher in the paclitaxel‐resistant Caski/Taxol cells compared with Caski cells (P < 0.05). Knockdown of FOXM1 significantly lowered the protein expression levels of FOXM1 and ABCC5. Intracellular paclitaxel concentrations were significantly higher amongst the Caski/Taxol cells following the knockdown of FOXM1 by shRNA or Siomycin A (P < 0.05). Conclusion. FOXM1 promotes drug resistance in cervical cancer cells by regulating ABCC5 gene transcription. The knockdown of FOXM1 with shRNA or Siomycin A promotes paclitaxel‐induced cell death by regulating ABCC5 gene transcription.

2Papers
8Collaborators