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Transgelin Depletion is Critical for the TGFβ1‐mediated Initiation of PLCγ1‐Cofilin‐driven Morphological and Migratory Changes in MDA‐MB‐231 Cells
Author(s) -
Raymundo Bernardo R.,
Oh InRok,
Kim MiJung,
Kim ChanWha
Publication year - 2019
Publication title -
bulletin of the korean chemical society
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.237
H-Index - 59
ISSN - 1229-5949
DOI - 10.1002/bkcs.11900
Subject(s) - gene knockdown , cofilin , microbiology and biotechnology , cytoskeleton , transforming growth factor , cell migration , signal transduction , biology , chemistry , actin cytoskeleton , cell culture , cell , biochemistry , genetics
The role of transgelin (TAGLN) in cancer has been discussed; however, the mechanisms underlying its regulation and correlation with MDA‐MB‐231 cell plasticity and migratory patterns remain unclear. We generated stable TAGLN‐knockdown MDA‐MB‐231 cells and treated them with phorbol 12‐myristate 13‐acetate or transforming growth factor (TGF)‐β. Chemotaxis, morphology, and invasion were assayed using three‐dimensional matrices to evaluate cytoskeletal remodeling and migratory changes. Wound healing assays were conducted using cell inserts. TAGLN knockdown cells exhibited altered morphology due to cytoskeletal remodeling, yet only untreated and TGFβ1‐treated cells exhibited enhanced migration. Untreated and TGFβ1‐treated TAGLN knockdown cells showed increased N‐WASP, ROCK1, and ROCK2 protein levels, which induce cytoskeletal remodeling. Evaluating phospholipase Cγ1 (PLCγ1)‐cofilin signaling‐related proteins revealed that only TGFβ1‐treated TAGLN knockdown cells were influenced by PLCγ1‐cofilin signaling. Taken together, TAGLN knockdown is necessary for the TGFβ1‐mediated activation of PLCγ1‐cofilin pathway‐driven amoeboid morphology and enhanced migratory properties in MDA‐MB‐231 cells.