2017
DOI: 10.1186/s12935-017-0443-5
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Regulatory effects of COL1A1 on apoptosis induced by radiation in cervical cancer cells

Abstract: BackgroundCervical cancer is a common cancer of women in developing countries, and radiotherapy still remains its predominant therapeutic treatment. Collagen type I alpha 1 (COL1A1) has been shown to have a radioresistance effect in previous studies. However, such effect of COL1A1 has not yet been revealed in cervical cancer.MethodsExpression of COL1A1 in cervical cancer tissues and normal tissues was assessed by qRT-PCR and immunohistochemistry. The effect of COL1A1 on radioresistance of human cervical cancer… Show more

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Cited by 53 publications
(46 citation statements)
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“…The results of the present study are in agreement with those of a previous study that demonstrated that there was elevated COL1A1 expression in cancer ( 54 ). A previous in vitro study also suggested that COL1A1 activity may promote cancer cell proliferation and/or invasion ( 7 ).…”
Section: Discussionsupporting
confidence: 93%
“…The results of the present study are in agreement with those of a previous study that demonstrated that there was elevated COL1A1 expression in cancer ( 54 ). A previous in vitro study also suggested that COL1A1 activity may promote cancer cell proliferation and/or invasion ( 7 ).…”
Section: Discussionsupporting
confidence: 93%
“…COL1A1 and COL4A1 are family members of human collagen genes. COL1A1 encodes the major component of fibrillar collagen found in most connective tissues, and involved in gap junction, cell proliferation and tumor invasion [ 42 , 43 ]. COL4A1 is an important flexible protein in the structure of the basement membranes interacted with nearby cells, playing a role in cell migration and growth [ 44 ].…”
Section: Discussionmentioning
confidence: 99%
“…Collagen can stimulate additional signaling pathways in cancer cells to exert various functions. The increased expression of COL1A1 affected the caspase-3/PI3K/AKT pathways to inhibit cell apoptosis in cervical cancer tissues [73]. After the withdrawal of rapamycin treatment, mutated COL1A1 reinforced PI3K-AKT-mammalian target of rapamycin (mTOR) signals in cancer stem cells to sustain the metastatic burden of ERα-positive breast cancer cells; however, lung metastases were independent of mTOR signaling [74].…”
Section: The Influence Of Collagen On Cancer Cell Behaviormentioning
confidence: 99%