<i>In vivo</i> and <i>in vitro</i> impact of miRNA-153 on the suppression of cell growth apoptosis through mTORC2 signaling pathway in breast cancer

Liu, Haimei; Zang, Hongyan; Kong, Jilin; Gong, Liguo

doi:10.1080/10799893.2021.1970766

Cited by 1 publication

(1 citation statement)

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“…In particular, Rictor activates caveolin 1 (Cav1) through the Akt signaling pathway to inhibit the apoptosis of GC cells ( 29 ). Liu et al ( 30 ) reported that real-time PCR and western blot showed that miR-153 downregulated the expression of Rictor, and this was related to the anti-tumor effect through increasing apoptosis and inhibiting the growth of breast cancer cells. A recent study ( 27 ) suggested that Rictor is a substrate for caspase-3 and is cleaved during apoptosis.…”

Section: General Biological Effects Of Rictor In Cancer Cellsmentioning

confidence: 99%

Roles of Rictor alterations in gastrointestinal tumors (Review)

Cao,

Guo,

Min

et al. 2024

Oncol Rep

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Gastrointestinal tumors account for five of the top 10 causes of mortality from all cancers (colorectal, liver, stomach, esophageal and pancreatic cancer). Mammalian target of rapamycin (mTOR) signaling is commonly dysregulated in various human cancers. As a core component of the mTOR complex 2 (mTORC2), Rictor is a key effector molecule of the PI3K/Akt pathway. A high alteration rate of Rictor has been observed in gastrointestinal tumors, and such Rictor alterations are often associated with resistance to chemotherapy and related adverse clinical outcomes. However, the exact roles of Rictor in gastrointestinal tumors remain elusive. The aim of the present study was to critically discuss the following: i) Mutation and biological characteristics of Rictor in tumors with a detailed overview of Rictor in cell proliferation, angiogenesis, apoptosis, autophagy and drug resistance; ii) the role of Rictor in tumors of the digestive system, particularly colorectal, hepatobiliary, gastric, esophageal and pancreatic cancer and cholangiocarcinoma; and iii) the current status and prospects of targeted therapy for Rictor by inhibiting Akt activation. Despite the growing realization of the importance of Rictor/mTORC2 in cancer, the underlying mechanistic details remain poorly understood; this needs to change in order for the development of efficient targeted therapies and re-sensitization of therapy-resistant cancers to be made possible.

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Section: General Biological Effects Of Rictor In Cancer Cellsmentioning

confidence: 99%