Prognostic implications of survivin and lung resistance protein in advanced non-small cell lung cancer treated with platinum-based chemotherapy

Huang, Wenfeng; Mao, Yan; Zhan, Yongzi; Huang, Jianfeng; Wang, Xiangping; Luo, Peng-Hui; Li, L I; Mo, Dun-Chang; Liu, Qiong; Xu, Huimin; Huang, Chien-Hung

doi:10.3892/ol.2015.3913

Cited by 15 publications

(16 citation statements)

References 34 publications

(34 reference statements)

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“…Survivin is also correlated with the poor prognosis of colorectal adenocarcinoma patients (13,(15)(16)(17)(18)(19). Survivin takes part in the cell apoptosis of gastric cancer cells (21,22), and is involved in cell cycle arrest in colorectal cancer (23).…”

Section: Discussionmentioning

confidence: 99%

“…Survivin, a member of the family of inhibitor of apoptosis (IAP) proteins, takes part in the inhibition of cell apoptosis, which is also related to the poor prognosis of various human cancers, including colorectal adenocarcinoma (13,(15)(16)(17)(18)(19). The survivin mRNA-circulating tumor cells are associated with prostate cancer metastasis (20).…”

Section: Introductionmentioning

confidence: 99%

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Knockdown of PARP6 or survivin promotes cell apoptosis and inhibits cell invasion of colorectal adenocarcinoma cells

Wang

Luo

et al. 2017

Oncology Reports

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Colorectal adenocarcinoma is the third most common cancer worldwide. PARP6, a novel member of the poly(ADP-ribose) polymerases (PARPs) and survivin, a member of the family of inhibitor of apoptosis (IAP) proteins are associated with a poor prognosis in various types of cancers. However, limited evidence exists regarding the interaction between PARP6 and survivin in colorectal adenocarcinoma. In the present study, we used the paired samples of 20 patients with colorectal adenocarcinoma to detect the expression of PARP6 and survivin in both tumor and adjacent normal colorectal mucosa. Their interaction and roles in cell viability, cell cycle, cell apoptosis and cell invasion were further investigated. Our results showed that both PARP6 and survivin exhibited higher expression in colorectal adenocarcinoma tissues and SW620 cells when compared with levels in adjacent non-tumor tissues and a normal colon cell line FHC. Co-immunoprecipitation assay showed that a significant correlation existed between PARP6 and survivin. We also showed that sole treatment of PARP6 siRNA or survivin siRNA partially inhibited the cell survival and invasion, induced cell G0/G1 arrest, and cell apoptosis at the early and late stages. The combined treatment of PARP6 siRNA and survivin siRNA suppressed the cell survival and cell invasion, further induced cell cycle phase G0/G1 arrest, and cell apoptosis at the early and late stages. Taken together, knockdown of PARP6 or survivin promotes cell apoptosis and inhibits the cell invasion of colorectal adenocarcinoma cells. A significant correlation exists between PARP6 and survivin, and both are promising targets for the development of new strategies for the diagnosis and treatment of advanced or metastatic colorectal adenocarcinoma.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Knockdown of PARP6 or survivin promotes cell apoptosis and inhibits cell invasion of colorectal adenocarcinoma cells

Wang

Luo

et al. 2017

Oncology Reports

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“…Furthermore, clinical studies have reported that LRP expression levels predict drug resistance and poor outcome in various types of cancer ( 30 , 31 ). LRP was identified as an independent prognostic factor for overall survival in advanced NSCLC treated with DDP-based chemotherapy ( 32 – 34 ).…”

Section: Discussionmentioning

confidence: 99%

Niclosamide enhances the cytotoxic effect of cisplatin in cisplatin-resistant human lung cancer cells via suppression of lung resistance-related protein and c-myc

et al. 2017

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Lung cancer is a leading cause of cancer-associated mortality worldwide. The cisplatin (DDP)-based chemotherapy remains the foundation of treatment for the majority of patients affected by advanced non-small cell lung cancer (NSCLC). However, DDP-resistance limits the clinical utility of this drug in patients with advanced NSCLC. The aim of the present study was to investigate the inhibitory effect of niclosamide on human lung cancer cell growth and to investigate the possible underlying mechanism. The effects of niclosamide on the proliferation of human lung adenocarcinoma (A549) and DDP-resistant (CR) human lung adenocarcinoma (A549/DDP) cells were examined by Cell Counting kit-8 assay. The impact of niclosamide on the apoptosis of A549/DDP cells was detected by Annexin V-fluorescein isothiocyanate/propidium iodide assay. The expression levels of cisplatin-resistant-associated molecules (lung resistance-related protein and c-myc) following niclosamide treatment in A549/DDP cells were evaluated by western blot analysis. The results indicated that niclosamide in combination with DDP demonstrated a synergistic effect in A549/DDP cells and directly induced apoptosis, which may be associated with caspase-3 activation. Furthermore, niclosamide decreased the expression level of c-myc protein, which may influence DDP sensitivity of A549/DDP cells. Thus, the present study indicates that niclosamide combined with DDP exerts a synergistic effect in cisplatin-resistant lung cancer cells and may present as a promising drug candidate in lung cancer therapy.

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“…MDR1 plays an important role in the development of drug resistance in cells, according to actively effluxes a wide array of anticancer drugs, including cisplatin and paclitaxel [ 33 ]. ERCC1 expression levels determined the sensitivity of cells to Pt in part [ 34 ], and LRP expression was associated with resistance to anti-cancer drugs including cisplatin, carboplatin, doxorubicin, etoposide and paclitaxel in vitro [ 35 ]. Expression of MDR1 was higher in A2780CP70 cells than that in A2780S cells.…”

Section: Resultsmentioning

confidence: 99%

Enhanced antitumor efficacy of cisplatin for treating ovarian cancer in vitro and in vivo via transferrin binding

et al. 2017

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Cisplatin is a widely used anticancer drug, while non-targeted delivery, development of drug resistance, and serious side effects significantly limit its clinical use. In order to improve the tumor-targeting properties of cisplatin, transferrin (Tf) was employed as a carrier to transfer cisplatin into cancer cells via transferrin receptor 1 (TfR1) mediated endocytosis. The binding ability of cisplatin and Tf could be improved by pretreating Tf with 10% ethanol, and the binding number of cisplatin for each Tf molecule could reach to 40 without structural or functional impairment of Tf. The Tf-cisplatin complex could be delivered into human ovarian carcinoma cells high efficiently. In tumor-bearing nude-mice model, the Tf-cisplatin complex inhibited tumor growth in vivo more effectively than free cisplatin, with less toxicity in other tissues. Tumor targeting efficiency of the Tf-cisplatin complex was supported by in vivo and ex vivo imaging and platinum residues detected in each ex vivo organ. These data suggested that Tf-cisplatin was more effective and less drug-resistance than cisplatin, with targeting to tumor cells. Therefore, Tf-mediated delivery of cisplatin is a potential strategy for targeted delivery into tumor cells.

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Prognostic implications of survivin and lung resistance protein in advanced non-small cell lung cancer treated with platinum-based chemotherapy

Cited by 15 publications

References 34 publications

Knockdown of PARP6 or survivin promotes cell apoptosis and inhibits cell invasion of colorectal adenocarcinoma cells

Knockdown of PARP6 or survivin promotes cell apoptosis and inhibits cell invasion of colorectal adenocarcinoma cells

Niclosamide enhances the cytotoxic effect of cisplatin in cisplatin-resistant human lung cancer cells via suppression of lung resistance-related protein and c-myc

Enhanced antitumor efficacy of cisplatin for treating ovarian cancer in vitro and in vivo via transferrin binding

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