The shift in GH3 cell shape and cell motility is dependent on MLCK and ROCK

Ávila-Rodríguez, Dulce; Agama, Carmen Solano; González-Pozos, Sirenia; Méndez-Méndez, Juan Vicente; Plata, Alma Ortiz; Arreola-Mendoza, Laura; Mendoza-Garrido, M. Eugenia

doi:10.1016/j.yexcr.2017.03.014

Cited by 8 publications

(4 citation statements)

References 60 publications

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“…There are many confounding factors of HFD‐induced hypertriglyceridemia in animal models, including weight gain, body composition, and the levels of hormones such as leptin, insulin, and ghrelin 21 . PA is the most abundant saturated fatty acid in the serum of HFD‐fed rats, 22 and GH3 is a well‐characterized pituitary cell line that synthesizes and secretes GH 23 . We treated GH3 cells with PA to survey whether lipotoxicity could directly suppress the synthesis of GH.…”

Section: Resultsmentioning

confidence: 99%

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Lipotoxicity suppresses the synthesis of growth hormone in pituitary somatotrophs via endoplasmic reticulum stress

Gong

Yang

Wei

et al. 2021

J Cellular Molecular Medi

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Section: Resultsmentioning

confidence: 99%

“…21 PA is the most abundant saturated fatty acid in the serum of HFD-fed rats, 22 and GH3 is a well-characterized pituitary cell line that synthesizes and secretes GH. 23 We treated GH3 cells with PA to survey whether lipotoxicity could directly suppress the synthesis of GH.…”

Section: Pa Directly Suppressed the Synthesis Of Gh In Gh3 Cellsmentioning

confidence: 99%

Lipotoxicity suppresses the synthesis of growth hormone in pituitary somatotrophs via endoplasmic reticulum stress

Gong

Yang

Wei

et al. 2021

J Cellular Molecular Medi

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show abstract

“…And statistical significance is indicated using asterisks (**p < 0.01, ***p < 0.001). MLCK is the primary protein promoting cell contractility [48], and MLC phosphorylation remarkably improves the migration and invasive abilities of GC cells [49]. Leiomyosarcomas, with high proliferative activity, exhibit high MLCK expression [50].…”

Section: Discussionmentioning

confidence: 99%

Melatonin Potentiates Sensitivity to 5-Fluorouracil in Gastric Cancer Cells by Upregulating Autophagy and Downregulating Myosin Light-Chain Kinase

Shi,

Li,

Dan

et al. 2023

J. Cancer

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5-Fluorouracil is an effective chemotherapeutic drug for gastric cancer. However, the acquisition of chemotherapeutic resistance remains a challenge in treatment. Melatonin can enhance the therapeutic effect of 5-fluorouracil; however, the underlying mechanisms are not well understood. We investigated the effects of combinations of melatonin and 5-fluorouracil on the proliferation, migration and invasion of gastric cancer cells. Melatonin significantly potentiated the 5-fluorouracil-mediated inhibition of proliferation, migration and invasion in gastric cancer cells, which potentiates sensitivity to 5-FU by promoting the activation of Beclin-1-dependent autophagy and targeting the myosin light-chain kinase (MLCK) signaling pathway. Previous studies have shown that autophagy might be associated with the MLCK signaling pathway. The autophagy inhibitor, 3-methyladenine, effectively rescued the migratory and invasive capabilities of gastric cancer cells, while also reducing expression level of MLCK and the phosphorylation level of MLC. This indicates that autophagy is involved in tumor metastasis, which may be related to inhibition of the MLCK signaling pathway. Our findings indicate that melatonin can improve the effectiveness of 5-fluorouracil in gastric cancer and could be used as a supplemental agent in the treatment of gastric cancer with 5-fluorouracil.

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“…MLCK confers the rat pituitary adenoma cells with a slow and directional motility (40), and phosphorylation of MLC markedly improves the invasion and migration ability of gastric cancer cells (41). Leiomyosarcoma patients with high expression of MLCK or p-MLC have shorter life spans than the patients with low expression of these proteins (42).…”

Section: Discussionmentioning

confidence: 99%

Fenretinide inhibits the proliferation and migration of human liver cancer HepG2 cells by downregulating the activation of myosin light chain kinase through the p38‑MAPK signaling pathway

et al. 2018

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N-(4-hydroxyphenyl)retinamide (4-HPR or fenretinide), which is a synthetic analog of all‑trans retinoic acid (ATRA), effectively inhibits the growth of several types of tumor cells; however, its molecular mechanism remains unclear. We found that 4‑HPR altered the morphology of human liver cancer HepG2 cells and also inhibited their proliferation and suppressed the colony formation in a dose‑ and time‑dependent manner. A wound healing assay revealed that 4‑HPR significantly hindered HepG2 cell migration, and that this was accompanied by the phosphorylation of p38‑MAPK (mitogen‑activated protein kinase). Mechanistically, the MAPK‑specific inhibitor SB203580 attenuated the inhibitory effects of 4‑HPR on the migration of HepG2 cells. Moreover, we also observed that 4‑HPR inhibited the activation and expression of myosin light chain kinase (MLCK) in HepG2 cells. Simultaneously, 4‑HPR lowered the expression of F‑actin and promoted the expression of E‑cadherin. ML‑7, a selective inhibitor of MLCK, significantly inhibited the migration of HepG2 cells while increasing the phosphorylation of p38‑MAPK and the expression of E‑cadherin, and decreasing the activation of MLCK and the expression of F‑actin. In conclusion, 4‑HPR inhibited the proliferation and migration of HepG2 cells, and p38‑MAPK plays an important role in regulating these 4‑HPR effects by reducing the activation of MLCK. The present study suggests that 4‑HPR may be a potent antimetastatic agent.

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The shift in GH3 cell shape and cell motility is dependent on MLCK and ROCK

Cited by 8 publications

References 60 publications

Lipotoxicity suppresses the synthesis of growth hormone in pituitary somatotrophs via endoplasmic reticulum stress

Lipotoxicity suppresses the synthesis of growth hormone in pituitary somatotrophs via endoplasmic reticulum stress

Melatonin Potentiates Sensitivity to 5-Fluorouracil in Gastric Cancer Cells by Upregulating Autophagy and Downregulating Myosin Light-Chain Kinase

Fenretinide inhibits the proliferation and migration of human liver cancer HepG2 cells by downregulating the activation of myosin light chain kinase through the p38‑MAPK signaling pathway

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