TAGLN2 promotes the proliferation, invasion, migration and epithelial-mesenchymal transition of colorectal cancer cells by activating STAT3 signaling through ANXA2

Oncol Lett. 2021 Oct;22(4):737. doi: 10.3892/ol.2021.12998. Epub 2021 Aug 16.ABSTRACTColorectal cancer (CRC) is one of the leading causes of cancer-associated mortality worldwide and currently ranks third in the USA in terms of prevalence. Transgelin-2 (TAGLN2) was previously reported to serve as a tumor promoter in various types of cancer. The present study aimed to investigate the role of TAGLN2 in the progression of CRC and to determine the potential underlying mechanism. The expression level of TAGLN2 in CRC cells (HCT116, SNU-C1, LoVo and SW480) were first detected by reverse transcription quantitative PCR and western blotting. Following TAGLN2 knockdown through transfection with short hairpin (sh)RNAs against TAGLN2, CRC cell proliferation was determined using Cell Counting Kit-8 and 5'-ethynyl-2'-deoxyuridine assays. Cell migration and invasion were evaluated using wound healing and Transwell assays, respectively. The expression levels of matrix metalloproteinase (MMP)2, MMP9 and proteins associated with epithelial-mesenchymal transition (EMT), including N-cadherin (N-cad), vimentin, zinc finger E-box binding homeobox 2 (ZEB2) and E-cadherin (E-cad), were also evaluated by western blotting. Furthermore, following TAGLN2 overexpression and the use of signal transducer and activator of transcription 3 (STAT3) inhibitors to treat CRC cells, all the aforementioned biological parameters were evaluated. The potential relationship between annexin 2 (ANXA2) and STAT3 was confi...
Source: Oncology Letters - Category: Cancer & Oncology Authors: Source Type: research