Silencing of BAG3 inhibits the epithelial-mesenchymal transition in human cervical cancer

Song, Fei; Wang, Geng; Ma, Zhiyong; Ma, Yushu; Wang, Yingying

doi:10.18632/oncotarget.20726

Cited by 11 publications

(12 citation statements)

References 23 publications

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“…Previous reports also suggested that miR-206 can regulate different target genes to function in diverse cell processes, such as cell differentiation, proliferation, and apoptosis 14–16 . In addition, B-cell lymphoma 2 (Bcl-2)-associated athanogene 3 (BAG3) is also involved in multiple biological processes of CC, including cell proliferation, migration, and invasion 17 . However, the expression and role of the miR-206/BAG3 pathway in human CC are still elusive.…”

Section: Introductionmentioning

confidence: 99%

miR-206 Inhibits Cell Proliferation, Migration, and Invasion by Targeting BAG3 in Human Cervical Cancer

Wang

Tian

2018

oncol res

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miR-206 and Bcl-2-associated athanogene 3 (BAG3) have been suggested as important regulators in various cancer types. However, the biological role of miR-206 and BAG3 in cervical cancer (CC) remains unclear. We investigated the expressions and mechanisms of miR-206 and BAG3 in CC using in vitro and in vivo assays. In the present study, miR-206 expression was expressed at a lower level in CC tissues and cells than adjacent normal tissues and NEECs. By contrast, BAG3 mRNA and protein were expressed at higher levels in CC tissues and cells. Furthermore, miR-206 overexpression repressed cell proliferation, migration, and invasion in vitro, and the 3'-untranslated region (3'-UTR) of BAG3 was a direct target of miR-206. miR-206 overexpression also inhibited EGFR, Bcl-2, and MMP2/9 protein expression, but promoted Bax protein expression. Besides, BAG3 overexpression partially abrogated miR-206-inhibited cell proliferation and invasion, while BAG3 silencing enhanced miR-206-mediated inhibition. In vivo assay revealed that miR-206 repressed tumor growth in nude mice xenograft model. In conclusion, miR-206 inhibits cell proliferation, migration, and invasion by targeting BAG3 in human CC. Thus, miR-206-BAG3 can be used as a useful target for CC.

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Section: Introductionmentioning

confidence: 99%

miR-206 Inhibits Cell Proliferation, Migration, and Invasion by Targeting BAG3 in Human Cervical Cancer

Wang

Tian

2018

oncol res

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“…Several reports have suggested EMT regulation as a mechanism that promotes the development of aggressive phenotype by BIS (11,29,30). However, most previous reports only reported changes in the EMT phenomena as a result of quantitative changes in BIS, and specific details on how BIS can affect EMT have not been elucidated.…”

Section: Discussionmentioning

confidence: 99%

Implication of BIS in the Migration and Invasion of A549 Non-small Cell Lung Cancer Cells

et al. 2018

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“…Additionally, siRNA-mediated depletion of BAG3 inhibits epithelial-mesenchymal transition (EMT) in cervical cancer cell lines in vitro and reduced tumor sizes in xenograft mouse model in vivo. This was accompanied by reduction of the EMT-regulator Slug and N-Cadherin and MMP2 as marker protein for the mesenchymal state and an increase in E-Cadherin, indicating an epithelial state [58].…”

Section: Cervical Cancermentioning

confidence: 97%

“…In cervical cancer, BAG3 expression was shown to correlate with tumor grade [57,58]. Additionally, siRNA-mediated depletion of BAG3 inhibits epithelial-mesenchymal transition (EMT) in cervical cancer cell lines in vitro and reduced tumor sizes in xenograft mouse model in vivo.…”

Section: Cervical Cancermentioning

confidence: 99%

At the Crossroads of Apoptosis and Autophagy: Multiple Roles of the Co-Chaperone BAG3 in Stress and Therapy Resistance of Cancer

Kögel

Linder

Brunschweiger

et al. 2020

Cells

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BAG3, a multifunctional HSP70 co-chaperone and anti-apoptotic protein that interacts with the ATPase domain of HSP70 through its C-terminal BAG domain plays a key physiological role in cellular proteostasis. The HSP70/BAG3 complex determines the levels of a large number of selective client proteins by regulating their turnover via the two major protein degradation pathways, i.e. proteasomal degradation and macroautophagy. On the one hand, BAG3 competes with BAG1 for binding to HSP70, thereby preventing the proteasomal degradation of its client proteins. By functionally interacting with HSP70 and LC3, BAG3 also delivers polyubiquitinated proteins to the autophagy pathway. BAG3 exerts a number of key physiological functions, including an involvement in cellular stress responses, proteostasis, cell death regulation, development, and cytoskeletal dynamics. Conversely, aberrant BAG3 function/expression has pathophysiological relevance correlated to cardiomyopathies, neurodegeneration, and cancer. Evidence obtained in recent years underscores the fact that BAG3 drives several key hallmarks of cancer, including cell adhesion, metastasis, angiogenesis, enhanced autophagic activity, and apoptosis inhibition. This review provides a state-of-the-art overview on the role of BAG3 in stress and therapy resistance of cancer, with a particular focus on BAG3-dependent modulation of apoptotic signaling and autophagic/lysosomal activity.

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Silencing of BAG3 inhibits the epithelial-mesenchymal transition in human cervical cancer

Cited by 11 publications

References 23 publications

miR-206 Inhibits Cell Proliferation, Migration, and Invasion by Targeting BAG3 in Human Cervical Cancer

miR-206 Inhibits Cell Proliferation, Migration, and Invasion by Targeting BAG3 in Human Cervical Cancer

Implication of BIS in the Migration and Invasion of A549 Non-small Cell Lung Cancer Cells

At the Crossroads of Apoptosis and Autophagy: Multiple Roles of the Co-Chaperone BAG3 in Stress and Therapy Resistance of Cancer

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