Neoplastic Reversal of Human Ovarian Carcinoma Cells Transfected with Connexin43

Fernström, Martha J.; Koffler, Lucas D.; Abou-Rjaily, George A.; Boucher, Paul D.; Shewach, Donna S.; Ruch, Randall J.

doi:10.1006/exmp.2002.2436

Cited by 24 publications

(16 citation statements)

References 22 publications

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“…However, inhibition gap junction function by a-GA led to an increase in drug resistance in ACRP. This finding is consistent with reports that overexpression of Cx43 in ovarian cancer cells can sensitize these cells to drug treatment (Fernstrom et al, 2002), and fits in the overall model that gap junction may have a role in transmitting the cell damage or death signals to neighboring cells, thereby causing a 'bystander' effect (Azzam et al, 1998;Tanaka et al, 2001). More difficult to explain is the fact that Cx43 is highly elevated in our cisplatin-resistant cell line ACRP, although Cx43 overexpression has been reported in cells subjected to various stresses (Azzam et al, 2003).…”

Section: Discussionsupporting

confidence: 91%

Gene expression response to cisplatin treatment in drug-sensitive and drug-resistant ovarian cancer cells

Wood

Becker

et al. 2006

Oncogene

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Section: Discussionsupporting

confidence: 91%

Gene expression response to cisplatin treatment in drug-sensitive and drug-resistant ovarian cancer cells

Wood

Becker

et al. 2006

Oncogene

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“…In human ovarian cancer cells, Cx43 overexpression has been shown to decrease cell proliferation and increase sensitivity to anti-cancer drugs [17][18][19]. Thus, Cx43 is believed to be a tumor suppressor in ovarian cancer.…”

Section: Discussionmentioning

confidence: 99%

“…Compared with human ovarian surface epithelium, Cx43 expression levels are significantly down-regulated in human ovarian cancer cells [15,16]. Overexpression of Cx43 in the SKOV3 human ovarian cancer cell line has been shown to decrease cell proliferation and tumor formation in nude mice [17]. In addition, ovarian cancer cells with high Cx43 expression are more sensitive to cisplatin and paclitaxel treatments [18,19].…”

Section: Introductionmentioning

confidence: 99%

Transforming growth factor-β stimulates human ovarian cancer cell migration by up-regulating connexin43 expression via Smad2/3 signaling

Qiu

Cheng

Zhao

et al. 2015

Cellular Signalling

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“…Combination therapy using the Cx gene and chemotherapeutic agents for cancer has been reported. Cx43 transfected into human glioblastoma cells (20) and ovarian carcinoma cells (21) led to the down-regulation of Bcl-2 and increased sensitivity to paclitaxel and doxorubicin. In our study, DTX treatment caused an increase in G 2 /M populations into PC-3 cells (Fig.…”

Section: Discussionmentioning

confidence: 99%

Combination of non-viral connexin 43 gene therapy and docetaxel inhibits the growth of human prostate cancer in mice

Fukushima

Hattori²,

Yoshizawa³

et al. 2007

Int J Oncol

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Abstract. Docetaxel (DTX) is used for the treatment of advanced hormone refractory prostate cancer. Connexin 43 (Cx43) is a tumor suppressor gene, and transfection of the Cx43 gene increases sensitivity to several chemotherapeutic agents. The objective of this study was to evaluate the effectiveness of combination therapy of Cx43-expressing plasmid DNA (pCMV-Cx43) and DTX both in vitro and in vivo using a non-viral vector in human prostate cancer PC-3 cells. Transfection of pCMV-Cx43 into the cells neither inhibited tumor growth nor increased gap junctional intercellular communication; however, combination therapy of pCMVCx43 and DTX significantly inhibited cell growth. Forced expression of Cx43 in the cells induced apoptotic cells by down-regulation of Bcl-2 expression and significantly more up-regulation of caspase-3 activity than either treatment alone. The combination of repeated intratumoral injection of pCMV-Cx43 (10 μg/tumor) with non-viral vector and a single intravenous injection of DTX (15 mg/kg) was compared with a repeated injection of Cx43 alone and a single injection of DTX alone on PC-3 tumor xenografts. Significant antitumoral effects were observed in mice receiving combined treatment, compared with DTX alone. The data presented here provide a rational strategy for treating patients with advanced hormone refractory prostate cancer.

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Neoplastic Reversal of Human Ovarian Carcinoma Cells Transfected with Connexin43

Cited by 24 publications

References 22 publications

Gene expression response to cisplatin treatment in drug-sensitive and drug-resistant ovarian cancer cells

Gene expression response to cisplatin treatment in drug-sensitive and drug-resistant ovarian cancer cells

Transforming growth factor-β stimulates human ovarian cancer cell migration by up-regulating connexin43 expression via Smad2/3 signaling

Combination of non-viral connexin 43 gene therapy and docetaxel inhibits the growth of human prostate cancer in mice

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