AICAR‐induced activation of AMPK inhibits the migration of TSCC cells by targeting ZO‐1

Guo, Xingyi; Lai, Xiao-Jin; Cai, Xinlei; Yuan, Peng; Wu, Fenghua; Yin, Mingzhu; Li, Yang; Zhang, Jun-Lin; Zhao, Gang

doi:10.1111/odi.13212

Cited by 2 publications

(1 citation statement)

References 13 publications

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“…In addition to its role in metabolism, AMPK is closely related to cell migration and plays diverse roles in different cells and environments [17]. Studies have shown that the activation of AMPK inhibits the migration of tongue squamous cell carcinoma cells [18]. Loss of AMPK activation promotes the invasion and metabolism in many cancers [15,19].…”

Section: Introductionmentioning

confidence: 99%

Electric field down-regulates CD9 to promote keratinocytes migration through AMPK pathway

Ji¹,

Teng²,

Zhang³

et al. 2020

Int. J. Med. Sci.

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Endogenous electric field (EF)-directed keratinocytes migration is known to play a key role in the wound re-epithelialization process. Although many molecules and signaling pathways are reported important for directional keratinocytes migration under EF, the underlying mechanism remains unclear. Our previous research found that CD9, a trans-membrane protein, is involved in wound re-epithelialization and CD9 downregulation contributes to keratinocytes migration. In this study, we observed the effect of EF on CD9 expression and keratinocytes migration. The keratinocytes migrated directionally toward the cathode and CD9 expression was down-regulated under EF (200mV/mm). In addition, CD9 overexpression reversed EF-induced migratory speed and the electrotactic response of keratinocytes. Also, we found that EF reduced AMP-activated protein kinase (AMPK) activity. Furthermore, AICAR, an AMPK activator, increased CD9 expression under EF, while compound C, an AMPK inhibitor, decreased CD9 expression in keratinocytes. Our results demonstrate that EF regulates CD9 expression and keratinocytes directional migration, in which AMPK pathway plays an important role.

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Section: Introductionmentioning

confidence: 99%

Electric field down-regulates CD9 to promote keratinocytes migration through AMPK pathway

Ji¹,

Teng²,

Zhang³

et al. 2020

Int. J. Med. Sci.

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The activation of adenosine monophosphate–activated protein kinase inhibits the migration of tongue squamous cell carcinoma cells by targeting Claudin‐1 via epithelial–mesenchymal transition

Zhou,

Liu,

et al. 2024

Anim Models and Exp Med

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BackgroundThe role of Claudin‐1 in tongue squamous cell carcinoma (TSCC) metastasis needs further clarification, particularly its impact on cell migration. Herein, our study aims to investigate the role of Claudin‐1 in TSCC cell migration and its underlying mechanisms.Methods36 TSCC tissue samples underwent immunohistochemical staining for Claudin‐1. Western blotting and immunofluorescence analyses were conducted to evaluate Claudin‐1 expression and distribution in TSCC cells. Claudin‐1 knockdown cell lines were established using short hairpin RNA transfection. Migration effects were assessed through wound healing assays. Furthermore, the expression of EMT‐associated molecules was measured via western blotting.ResultsClaudin‐1 expression decreased as TSCC malignancy increased. Adenosine monophosphate–activated protein kinase (AMPK) activation led to increased Claudin‐1 expression and membrane translocation, inhibiting TSCC cell migration and epithelial–mesenchymal transition (EMT). Conversely, Claudin‐1 knockdown reversed these inhibitory effects on migration and EMT caused by AMPK activation.ConclusionsOur results indicated that AMPK activation suppresses TSCC cell migration by targeting Claudin‐1 and EMT pathways.

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AICAR‐induced activation of AMPK inhibits the migration of TSCC cells by targeting ZO‐1

Cited by 2 publications

References 13 publications

Electric field down-regulates CD9 to promote keratinocytes migration through AMPK pathway

Electric field down-regulates CD9 to promote keratinocytes migration through AMPK pathway

The activation of adenosine monophosphate–activated protein kinase inhibits the migration of tongue squamous cell carcinoma cells by targeting Claudin‐1 via epithelial–mesenchymal transition

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