MTA2 (Metastasis Associated 1 Family Member 2)

In this context, we summarize linked function of MTA2 directly to oncogenesis and might provide a significant avenue for the treatment of diseases. We hope that this review will help tumor molecular biologists further understand the molecular mechanism of MTA2 in normal development and cancer.

Taken together, these findings highlight that HMGB2 plays a crucial role in promoting heart regeneration through regulating glycolysis. Activating the HMGB2-MTA2-HIF-1α axis might serve as a potential therapeutic option for regenerative therapies post-myocardial injury.

Treatment of MIA PaCa-2 cells with AS1411-Lipm[siRNA] significantly reduced MTA2 expression by ~60%, substantially restored PTEN, and inhibited AKT phosphorylation by ~50%, leading to decreased cell viability, impaired migration by ~75%, and increased apoptosis by ~35%, while sparing nucleolin-negative cells. These findings highlight AS1411-Lipm[siRNA] as a promising platform for selective siRNA delivery and potent molecular inhibition in PDAC therapy.

Although adult Mta3ΔBAHanimals did not exhibit androgen dysregulation, Mta3ΔBAHmales displayed sex-dependent behaviors suggesting dysregulation during critical windows of behavioral development. These studies clarify the genetic requirements for MTA proteins in mammalian development and identify specific functions for MTA3.

 The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 4899‑4908, 2018; DOI: 10.3892/mmr.2018.8535].

HIF-1α could inhibit the proliferation, invasion and metastasis of nasopharyngeal carcinoma by regulating the expression of MMP-2, thus inhibiting tumor growth. Therefore, HIF-1α and MMP-2 might become important therapeutic targets to inhibit the growth, invasion and metastasis of nasopharyngeal carcinoma.

Overall, our study suggests that MTA2 knockdown suppresses osteosarcoma cell metastasis by decreasing uPA expression via ERK signaling. This finding provides new insight into potential treatment strategies against osteosarcoma metastasis by targeting MTA2.

Clones with mutations in these genes grow in frequency and size with age, comparable to classical CH drivers. They correlate with heightened risk of infection, death and hematological malignancy, highlighting the significance of these additional genes in the aging process.

Based on multi-omics data and ML algorithms, we successfully developed the ISRS to enable accurate diagnosis and prognostic stratification in NB, which shed light on molecular mechanisms of spontaneous regression and clinical utilization of ISRS.

Taken together, these findings uncover that circMTA2 suppresses MTA2 degradation by interacting with UCHL3, thereby promoting GC progression. In conclusion, we identified a cancer-promoting axis (circMTA2/UCHL3/MTA2) in GC progression, which paves the way for us to design and synthesize targeted inhibitors as well as combination therapies.

Furthermore, deactivation of FAK using siFAK or FAK inhibitor (PF-573228, PF) synergistically contributed to PTK7 knockdown-inhibited FAK activity, MMP7 expression, and the migration and invasion abilities of HCC cells. Collectively, our findings show that PTK7 mediates HCC progression by regulating the MTA2-FAK-MMP7 axis and may be a diagnostic value for HCC patients.