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.

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Objective. To evaluate the diagnostic value of the nanometer carbon suspension tracer staining technique in sentinel lymph node biopsy of breast cancer is the objective of this study. Methods. The PubMed, Embase, Cochrane Library (Central), and Web of Science (SCI Expanded), and Chinese databases (CNKI, VIP, Wan Fang, and CBM) were systematically searched for studies on the diagnostic value of nanocarbon suspension in sentinel lymph node biopsy of breast cancer. Two reviewers independently assessed the methodological quality of each study using the QUADAS-2 tool. The extracted valid data were calculated using Meta-Disc1.4 software and tested for heterogeneity. STATA14.0 software was selected for sensitivity analysis of the included studies, and publication bias was assessed using Deeks’ forest plot asymmetry test. Results. A total of 10 studies were obtained. The pooled data were as follows: sensitivity, 0.92 (0.88~0.95); specificity, 0.99 (0.98~1.00); positive likelihood ratio, 69.24 (30.34~158.02); negative likelihood ratio, 0.09 (0.06~0.13); and the combined diagnostic odds ratio, 747.40 (285.77~1954.76), AUC = 0.9881 . Nanocarbon suspension tracers have an accuracy rate of 98.81% in the diagnosis of sentinel lymph nodes in breast cancer. Conclusion. Tracer staining technology based on nanocarbon suspension can accurately assess the status of lymph nodes in sentinel lymph node biopsy of breast cancer and has good stability and operability, which is worthy of clinical promotion.