MTA1, a metastasis‑associated protein, in endothelial cells is an essential molecule for angiogenesis

Ishikawa, Mizuho; Osaki, Mitsuhiko; Uno, Narumi; Ohira, Takahito; Kugoh, Hiroyuki; Okada, Futoshi

doi:10.3892/mmr.2021.12527

Cited by 2 publications

(1 citation statement)

References 31 publications

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“…The anti‐angiogenic effect of GnC may in part be linked to MTA1 inhibition since MTA1 association with angiogenesis is well recognized. [ 23,60,74–77 ] In addition, induction of apoptosis was much stronger with the combination treatment than with either compound alone. Moreover, when the underlying molecular pathways were investigated, AR‐V7 and MTA1 levels were significantly attenuated by GnC alone and in combination with Enz, showing the beneficial effects of combined treatment.…”

Section: Discussionmentioning

confidence: 99%

Molecular Efficacy of Gnetin C as Dual‐Targeted Therapy for Castrate‐Resistant Prostate Cancer

Campanelli,

Deabel,

Puaar

et al. 2023

Molecular Nutrition Food Res

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ScopeResistance of castrate‐resistant prostate cancer (CRPC) to enzalutamide (Enz) involves the expression of constitutively active androgen receptor splice variant (AR‐V7). In addition to altered AR pathways, CRPC is characterized by “non‐AR‐driven” signaling, which includes an overexpression of metastasis‐associated protein 1 (MTA1). Combining natural compounds with anticancer drugs may enhance drug effectiveness while reducing adverse effects. In this study, the in vitro and in vivo anticancer effects of Gnetin C (GnC) alone and in combination with Enz against CRPC are examined.Methods and resultsThe effects of GnC alone and in combination with Enz are assessed by cell viability, clonogenic survival, cell migration, and AR and MTA1 expression using 22Rv1 cells. The tumor growth in vivo is assessed by bioluminescent imaging, western blots, RT‐PCR, and IHC. GnC alone and in combined treatment inhibit cell viability, clonogenic survival and migration, and AR and MTA1 expression in 22Rv1 cells. The underlying AR‐ and MTA1‐targeted anticancer mechanisms of treatments in vivo involve inhibition of proliferation and angiogenesis, and induction of apoptosis.ConclusionThe findings demonstrate that GnC alone and GnC combined with Enz effectively inhibits AR‐ and MTA1‐promoted tumor‐progression in advanced CRPC, which indicates its potential as a novel therapeutic approach for CRPC.

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Section: Discussionmentioning

confidence: 99%

Molecular Efficacy of Gnetin C as Dual‐Targeted Therapy for Castrate‐Resistant Prostate Cancer

Campanelli,

Deabel,

Puaar

et al. 2023

Molecular Nutrition Food Res

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MTA1: A Vital Modulator in Prostate Cancer

Qian

et al. 2022

CPPS

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Prostate cancer (PCa) is the most frequent cancer of the male genitourinary system and the second most common cancer in men worldwide. PCa has become one of the leading diseases endangering men's health in Asia in recent years, with a large increase in morbidity and mortality. MTA1 (metastasis-associated antigen-1), a transcriptional coregulator involved in histone deacetylation and nucleosome remodeling, is a member of the MTA family. MTA1 is involved in cell signaling, chromosomal remodeling, and transcriptional activities, all of which are important for epithelial cell progression, invasion, and growth. MTA1 has been demonstrated to play a significant role in the formation, progression, and metastasis of PCa, and MTA1 expression is specifically linked to PCa bone metastases. Therefore, MTA1 may be a potential target for PCa prevention and treatment. Here, we reviewed the structure, function, and expression of MTA1 in PCa as well as drugs that target MTA1 to highlight a potential new treatment for PCa.

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MTA1, a metastasis‑associated protein, in endothelial cells is an essential molecule for angiogenesis

Cited by 2 publications

References 31 publications

Molecular Efficacy of Gnetin C as Dual‐Targeted Therapy for Castrate‐Resistant Prostate Cancer

Molecular Efficacy of Gnetin C as Dual‐Targeted Therapy for Castrate‐Resistant Prostate Cancer

MTA1: A Vital Modulator in Prostate Cancer

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