Suppression of human MDA-MB-435S tumor by U6 promoter-driven short hairpin RNAs targeting focal adhesion kinase

Huang, Anliang; Wan, Yang; Liao, Dian‐ying; Huo-zhen, HU; Lin, Wei; Li, Linyu; Wang, Yuming; Li, Jiong; Chen, Lijuan; Kan, Bing; Chen, Ping; Wang, Yongsheng; Chen, Xiang; Zhao, Xia; Deng, Hongxin; Wei, Yuquan

doi:10.1007/s00432-010-0773-3

Cited by 3 publications

(4 citation statements)

References 52 publications

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“…7 Various studies have indicated that down-regulation of focal adhesion kinase expression may represent a potential therapeutic approach, retarding the unlimited proliferation and apoptosis suppression seen in various neoplasms such as malignant glioma, colon carcinoma and breast cancer. [4][5][6] However, the effect of focal adhesion kinase on cellular apoptosis and proliferation within laryngeal squamous cell carcinoma still remains unclear. In the current study, we investigated whether focal adhesion kinase contributes to apoptosis inhibition and proliferation promotion in laryngeal cancer, by assessing focal adhesion kinase expression in laryngeal cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…3 Previous studies have demonstrated that focal adhesion kinase is involved in regulating cellular proliferation in several different types of tumours. [4][5][6] Other authors have found that focal adhesion kinase influences cell apoptosis in a variety of tumours. 4,5,7,8 To the best of our knowledge, no previous studies have assessed the in vivo relationship between focal adhesion kinase expression and cellular proliferation and apoptosis within laryngeal squamous cell carcinoma.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Involvement of focal adhesion kinase in cellular proliferation, apoptosis and prognosis of laryngeal squamous cell carcinoma

Sun

et al. 2012

J. Laryngol. Otol.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Involvement of focal adhesion kinase in cellular proliferation, apoptosis and prognosis of laryngeal squamous cell carcinoma

Sun

et al. 2012

J. Laryngol. Otol.

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“…In this study, the gene delivery system we utilized was the same as previously reported (35,36), which proved to efficiently increase the therapeutic efficacy of the survivinT34A plasmid. Our previous biodistribution studies have showed that cationic lipid-DNA complexes was accumulated mainly in tumor tissues (37). This is due to the leaky microvasculature in tumors that could facilitate extravasation, and thus, increase the permeability of tumor vessels to liposomes.…”

Section: Discussionmentioning

confidence: 99%

SurvivinT34A increases the therapeutic efficacy of arsenic trioxide in mouse hepatocellular carcinoma models

et al. 2016

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Arsenic trioxide (ATO) has demonstrated clinical efficacy in acute promyelocytic leukemia (APL) and in vitro activity in various solid tumors. As2O3 as single agent exhibits poor efficacy for treatment of hepatocellular carcinoma (HCC) in phase II trial, suggesting that new modalities of treatment with enhanced therapeutic effect and alleviated toxicity are needed for application of As2O3 on patients with HCC. Survivin is the strongest inhibitor of apoptosis protein over-expressed in tumors, which has been proposed as an attractive target for new anticancer interventions. Disruption of survivin by the plasmid encoding the phosphorylation-defective mouse survivin threonine 34→alanine mutant (Msurvivin T34A plasmid) has proved a promising strategy for suppressing a variety of murine cancer. In the present study, we attempted to test Msurvivin T34A and arsenic trioxide (ATO) on a cell line and mice bearing subcutaneous tumors, with regard to their effects and mechanisms. We observed that the co-treatment with surivinT34A and ATO significantly enhanced the antitumor activity by induction of apoptosis in Hepa1-6 tumor cells in vitro, compared with control groups. The synergistic apoptosis-inducing effect of combination of these two drugs resulted in elevation of reactive oxygen species (ROS) level which could be antagonized by the antioxidant N-acetyl-l-cysteine. The combination treatment induced ROS-dependent collapse of the mitochondrial membrane potential. Moreover, the tumor growth in vivo was also remarkably inhibited by combination of surivinT34A and ATO when compared with control groups. Our findings demonstrate that the combination of surivinT34A and ATO exerted synergistic antitumor effects, providing a new perspective for clinical treatment of HCC.

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“…FAK activity can be altered, and its expression can be usually up-regulated in tumors [6][7][8]. FAK inhibition could result in cell detached [9], apoptotic [10,11], decrease cell proliferation [12], migration [13] and invasion [10,14]. Moreover, the up-regulated FAK could enhance tumor metastasis and cause the poor prognosis for patients [14][15][16], and it was also reported may be closely associated with the development of the malignant phenotypes in colorectal carcinoma and hepatocellular carcinoma [14,17].…”

Section: Introductionmentioning

confidence: 99%

The effects of focal adhesion kinase on the motility, proliferation and apoptosis of Caco2 and SMMC-7721 cells

Gao

et al. 2015

Med Oncol

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Focal adhesion kinase (FAK) plays important roles in cancer development. However, the significance of FAK expression in colorectal carcinoma and hepatocellular carcinoma has not been clarified. This study aims to explore the roles FAK played in the progression of colorectal carcinoma and hepatocellular carcinoma. RNAi method was used to inhibit the expression of FAK in Caco2 and SMMC-7721 cells. Reverse transcriptase polymerase chain reaction analysis and Western blot analysis were used to examine mRNA and protein expression of FAK. Then, the proliferation, motility and apoptosis of both types of cells were detected using MTT assay, wound healing/transwell assay and nuclear staining assay. The microstructure changes (F-actin, β-tubulin and lamin B1) of SMMC-7721 cells were visualized by immunofluorescence. FAK was overexpressed in both cell lines and down-regulation of FAK resulted in suppression of cell proliferation, inhibition of cell migration and invasion. The apoptosis of cells was increased significantly following the FAK expression inhibition. Moreover, actin polymerization, β-tubulin and lamin B1 expression of cells were significantly decreased. The results highlight the role of FAK in the progression of cancers. These findings suggest FAK serve as a potential therapeutic target for cancer therapy.

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Suppression of human MDA-MB-435S tumor by U6 promoter-driven short hairpin RNAs targeting focal adhesion kinase

Abstract: These results indicate that the systemic delivery of plasmid DNA targeting FAK function using cationic liposome as a gene carrier, represents a promising avenue for breast cancer therapy.

Cited by 3 publications

References 52 publications

Involvement of focal adhesion kinase in cellular proliferation, apoptosis and prognosis of laryngeal squamous cell carcinoma

Involvement of focal adhesion kinase in cellular proliferation, apoptosis and prognosis of laryngeal squamous cell carcinoma

SurvivinT34A increases the therapeutic efficacy of arsenic trioxide in mouse hepatocellular carcinoma models

The effects of focal adhesion kinase on the motility, proliferation and apoptosis of Caco2 and SMMC-7721 cells

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