TAGLN2 promotes the proliferation, invasion, migration and epithelial‑mesenchymal transition of colorectal cancer cells by activating STAT3 signaling through ANXA2
- Zhicheng Zhao
- Li Lu
- Weidong Li
Affiliations: Department of General Surgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China
- Published online on: August 16, 2021 https://doi.org/10.3892/ol.2021.12998
Copyright: © Zhao
et al. This is an open access article distributed under the
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Commons Attribution License.
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Colorectal 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 confirmed by western blotting analysis. The expression level of TAGLN2 was found to be particularly high in CRC cells. Following TAGLN2 knockdown, CRC cell proliferation, migration, invasion and EMT were significantly inhibited. TAGLN2 knockdown also suppressed STAT3 phosphorylation in CRC cells. In addition, the promoting effects of TAGLN2 overexpression on the progression of CRC were reversed by STAT3 inhibitor. Furthermore, ANXA2 was positively associated with STAT3. Taken together, these findings demonstrated that TAGLN2 could promote the proliferation, invasion, migration and EMT of CRC cells by activating STAT3 and regulating ANXA2 expression. This may reveal the underlying mechanism by which TAGLN2 might regulate the progression of CRC and provide potential therapeutic targets for the treatment of CRC.