Overexpression of the Survivin gene in SGC7901 cell resistance to cisplatin

Abstract

The aim of the present study was to investigate the mechanism of SGC7901 cell resistance to cisplatin (CDDP). SGC7901/CDDP cells were established by the long-term continuous exposure of SGC7901 cells to CDDP in stepwise concentration increments. The morphologies of the SGC7901/CDDP and SGC7901 cells were observed by microscopy. The expression levels of Survivin mRNA and protein in the SGC7901/CDDP and SGC7901 cells were examined by reverse transcription polymerase chain reaction and western blotting respectively. The results revealed morphological differences between the SGC7901 and SGC7901/CDDP cells. The expression levels of Survivin mRNA and protein were significantly higher in the SGC7901/CDDP cells than in the SGC7901 cells. Therefore, high expression levels of the Survivin gene may explain SGC7901 cell resistance to CDDP.

SUVmax of 18F-FDG PET/CT correlates to expression of major chemotherapy-related tumor markers and serum tumor markers in gastric adenocarcinoma patients

“…Overexpression of it mainly indicates inhibition of apoptosis and cell cycle control (42). One study found that Survivin was a positive biomarker for predicting the sensitivity of paclitaxel treatment in gastric cancer patients by western blotting method, however, overexpression of Survivin was closely related with cisplatin and 5-FU treatment sensitivity in gastric SGC7901 cancer cells, and in nude mice, and knockdown of Survivin expression by shRNA, the cisplatin and 5-FU treatment sensitivity of gastric SGC7901 cancer cells and the nude mice enhanced significantly (13,43,44).…”

“…However, a large population remains resistant to chemotherapy, this suggests that there is still significant room for improvement of diagnosis and therapy in gastric adenocarcinoma patients (7,8). To our knowledge, it is clear that some patients who are positive of human epidermal growth factor receptor-2 (Her-2), P53 and Survivin will indicate poor prognosis due to chemotherapy resistance (9)(10)(11)(12)(13)(14). Therefore, the relationships between these chemotherapy-related biomarkers and the SUVmax of 18 F-FDG PET/CT are needed, to predict the occurrence of chemotherapy resistance and create personalized therapeutic regimens of gastric adenocarcinoma patients before chemotherapy treatment.…”

HDAC2 and HDAC5 Up-Regulations Modulate Survivin and miR-125a-5p Expressions and Promote Hormone Therapy Resistance in Estrogen Receptor Positive Breast Cancer Cells

“…Aberrant regulations of the Akt-mTOR-survivin and the p53/Sp1-survivin signaling pathways have widely been shown to promote the survival of cancer cells and the induction of anti-cancer drugs resistance ( Cheung et al, 2009 ; Coumar et al, 2013 ; Dong et al, 2014 ; Sun et al, 2014 ; Han et al, 2015 ; Parvani et al, 2015 ; Kim et al, 2016 ). It is not surprising to see that the HDAC2 up-regulated MCF7-TamC3 cells exhibit increased endogenous expression of survivin as compared to the parental hormone therapy-sensitive MCF7 cells because p53 is a negative transcription regulator of the survivin gene ( Mirza et al, 2002 ).…”

Targeting phosphorylation of STAT3 delays tumor growth in HPV-negative anal squamous cell carcinoma mouse model

“…Furthermore, the reversion of chemo-resistance was observed after STAT3 signaling had been blocked 18, 19 . Survivin also contributes to chemo-resistance in cancer patients, and its transcription was induced by the activation of STAT3 14, 15, 20 . These raised a question about whether the combination of STAT3 inhibitor and chemotherapy would have greater anti-tumor effects in ASCC mouse model.…”