Thrombocytosis and immunohistochemical expression of connexin 43 at diagnosis predict survival in advanced non-small-cell lung cancer treated with cisplatin-based chemotherapy

Du, Gangjun; Yang, Ya; Zhang, Yaping; Sun, Ting; Liu, Weijie; Wang, Yingying; Zhang, Houyun

doi:10.1007/s00280-013-2080-6

Cited by 30 publications

(27 citation statements)

References 23 publications

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“…Previous studies have indicated that Cx43 is able to sensitize cells to apoptosis in response to chemotherapeutic drugs through GJC (18,28); however, another study reported that the role of Cx43 in chemotherapy-induced apoptosis is independent of GJC function (12). The results of the MTT assay in the current study indicated a role for Cx43 in mediating the apoptosis of CRC cell lines.…”

Section: Discussionsupporting

confidence: 62%

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Connexin 43 enhances paclitaxel cytotoxicity in colorectal cancer cell lines

Wang¹,

Zhao²,

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Colorectal cancer has a relatively low sensitivity to paclitaxel. The purpose of this study was to investigate the role of connexin 43 (Cx43), which is a structural component of gap junctional communication (GJC), in paclitaxel cytotoxicity in colorectal cancer cells. Three colorectal cancer cell lines (HCT106, HCT116 and LoVo) were transfected with Cx43 and used to examine paclitaxel cytotoxicity. A western blot assay was used to confirm Cx43 expression in transfected cell lines as well as the expression of several proteins that are associated with paclitaxel cytotoxicity. A parachute dye-coupling assay was used to measure GJC function. An MTT assay was used to analyze the viability of paclitaxel-treated cells. Cx43 expression level and GJC function were significantly upregulated by the transfection (P<0.05). The viability of transfected cells was significantly inhibited compared with that of untransfected cells when treated with paclitaxel (20 or 80 nM) at high culture density but not at low culture density (P<0.05). Cx43 transfection significantly increased the mitotic arrest, tubulin polymerization and apoptosis effects of paclitaxel (P<0.05). It was also found that paclitaxel had an inhibitory effect on GJC function after 12 h of treatment in LoVo cells (P<0.05). These results indicate that Cx43 may serve as a target of paclitaxel chemotherapy for colorectal cancer.

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Section: Discussionsupporting

confidence: 62%

“…Previous studies have demonstrated that connexins, a group of tumor suppressor genes, are potential anti-oncogenic targets for chemotherapy, and the upregulation of connexin expression can increase sensitivity to antitumor drugs in many cancer types (12,13). Connexins form gap junctions, which are important intercellular channels.…”

Section: Introductionmentioning

confidence: 99%

Connexin 43 enhances paclitaxel cytotoxicity in colorectal cancer cell lines

Wang¹,

Zhao²,

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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“…Similarly recent studies tracking connexin levels as a cancer prognostic indicator produced a diverse set of outcomes. Over a dozen studies in the last decade correlate high connexin expression with a significantly better prognosis (e.g., Cx43 in prostate 39 , pancreatic 40 , breast 41 , head and neck SCC 42 , non-small-cell lung 43 , and colorectal 44 cancers; and Cx26 in colorectal 45 and intestinal type-gastric 46 cancers). In contrast, more than a dozen studies correlate high connexin expression with a poor prognosis (e.g., Cx43 in oral SCC 47 , esophageal SCC 48 and non-muscle invasive urothelial bladder cancer 49 ; and Cx26 in breast cancer 50,51 , lung SCC 52 , esophageal SCC 53 , colorectal cancer 37 and papillary and follicular thyroid cancer 54 ).…”

Section: Expression and Localizationmentioning

confidence: 99%

Gap junctions and cancer: communicating for 50 years

et al. 2016

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Fifty years ago, tumour cells were found to lack electrical coupling, leading to the hypothesis that loss of direct intercellular communication is commonly associated with cancer onset and progression. Subsequent studies linked this phenomenon to gap junctions composed of connexin proteins. While many studies support the notion that connexins are tumour suppressors, recent evidence suggests that, in some tumour types, they may facilitate specific stages of tumour progression through both junctional and non-junctional signalling pathways. This Timeline article highlights the milestones connecting gap junctions to cancer, and underscores important unanswered questions, controversies and therapeutic opportunities in the field.

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“…Studies have shown that Cx43 plays important roles in cancer development, cell proliferation, apoptosis, invasion and metastasis in lung cancer (20)(21)(22)(23)(24)(25)(26). Most importantly, Cx43 is able to sensitize NSCLC cells to CDDP and ionizing radiation (27,28).…”

Section: Introductionmentioning

confidence: 99%

Cx43 reverses the resistance of A549 lung adenocarcinoma cells to cisplatin by inhibiting EMT

Zhang

et al. 2014

Oncology Reports

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Cisplatin (CDDP) is one of the standard first-line chemotherapeutic agents for advanced non-small cell lung cancer (NSCLC). Unfortunately, prolonged exposure to CDDP results in acquired resistance which prevents the successful treatment of lung cancer patients. Thus, it is necessary to explore the mechanism underlying the resistance of NSCLC to CDDP. In the present study, a CDDP-resistant human lung cancer cell line A549/CDDP was established from the parental cell line A549. The results demonstrated that A549/CDDP cells acquired an epithelial-mesenchymal transition (EMT) phenotype, with morphological changes including acquisition of a spindle-like fibroblastic phenotype, downregulation of E-cadherin, upregulation of mesenchymal markers (vimentin, Snail and Slug), and increased capability of invasion and migration. Compared with A549 cells, the A549/CDDP cells showed decreased connexin43 (Cx43) expression. Overexpression of Cx43 reversed EMT and CDDP resistance in the A549/CDDP cells. Conversely, knockdown of Cx43 expression by siRNA-Cx43 initiated EMT and induced CDDP insensitivity in A549 cells. In summary, Cx43 reverses CDDP resistance in A549 CDDP-resistant cells by preventing EMT, making Cx43 a possible therapeutic target for lung cancer.

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Thrombocytosis and immunohistochemical expression of connexin 43 at diagnosis predict survival in advanced non-small-cell lung cancer treated with cisplatin-based chemotherapy

Cited by 30 publications

References 23 publications

Connexin 43 enhances paclitaxel cytotoxicity in colorectal cancer cell lines

Connexin 43 enhances paclitaxel cytotoxicity in colorectal cancer cell lines

Gap junctions and cancer: communicating for 50 years

Cx43 reverses the resistance of A549 lung adenocarcinoma cells to cisplatin by inhibiting EMT

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