The mechanistic target of rapamycin (mTOR) coordinates eukaryotic cell growth and metabolism with environmental inputs, including nutrients and growth factors. Extensive research over the past two decades has established a central role for mTOR in regulating many fundamental cell processes, from protein synthesis to autophagy, and deregulated mTOR signaling is implicated in the progression of cancer and diabetes, as well as the aging process. Here, we review recent advances in our understanding of mTOR function, regulation, and importance in mammalian physiology. We also highlight how the mTOR signaling network contributes to human disease and discuss the current and future prospects for therapeutically targeting mTOR in the clinic.

mTOR Signaling in Growth, Metabolism, and Disease

miR-1273g silences MAGEA3/6 to inhibit human colorectal cancer cell growth via activation of AMPK signaling.

In recent years, gene editing, especially that using clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9, has made great progress in the field of gene function. Rapid development of gene editing techniques has contributed to their significance in the field of medicine. Because the CRISPR/Cas9 gene editing tool is not only powerful but also has features such as strong specificity and high efficiency, it can accurately and rapidly screen the whole genome, facilitating the administration of gene therapy for specific diseases. In the field of tumor research, CRISPR/Cas9 can be used to edit genomes to explore the mechanisms of tumor occurrence, development, and metastasis. In these years, this system has been increasingly applied in tumor treatment research. CRISPR/Cas9 can be used to treat tumors by repairing mutations or knocking out specific genes. To date, numerous preliminary studies have been conducted on tumor treatment in related fields. CRISPR/Cas9 holds great promise for gene-level tumor treatment. Personalized and targeted therapy based on CRISPR/Cas9 will possibly shape the development of tumor therapy in the future. In this study, we review the findings of CRISPR/Cas9 for tumor treatment research to provide references for related future studies on the pathogenesis and clinical treatment of tumors.

Application of CRISPR/Cas9 gene editing technique in the study of cancer treatment.

The PP2A subunit PR130 is a key regulator of cell development and oncogenic transformation

https://www.researchsquare.com/article/rs-573782/v1.pdf?c=1631898324000

Targeting PP2A with lomitapide suppresses colorectal tumorigenesis through the activation of AMPK/Beclin1-mediated autophagy.

// Cuiping Dai 1 , Xuning Zhang 2, * , Da Xie 3 , Peipei Tang 2 , Chunmei Li 2 , Yi Zuo 4 , Baofei Jiang 5 and Caiping Xue 2 1 Faculty of Health, Jiangsu Food and Pharmaceutical Science College, Huaian, China 2 Huaian Key Laboratory Of Gastrointestinal Cancer, Jiangsu College of Nursing, Huaian, China 3 Oncology Department, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China 4 Department of Medicine, Xinglin College, Nantong University, Nantong, China 5 Gastrointestinal Surgery, The First People’s Hospital of Huaian City, Huaian, China * Co-first author Correspondence to: Caiping Xue, email: xuecplwtg@163.com ; hywxxcp@163.com Baofei Jiang, email: slhjliangcq@163.com Keywords: protein phosphatase 2A (PP2A); LB-100; colorectal cancer (CRC); AMP-activated protein kinase (AMPK) and mTOR Received: August 01, 2017     Accepted: August 24, 2017     Published: September 28, 2017 ABSTRACT LB-100 is a novel PP2A inhibitor. Its activity in human colorectal cancer (CRC) cells was tested. The in vitro studies demonstrated that LB-100 inhibited survival and proliferation of both established CRC cells (HCT-116 and HT-29 lines) and primary human colon cancer cells. Further, LB-100 activated apoptosis and induced G1-S cell cycle arrest in CRC cells. LB-100 inhibited PP2A activity and activated AMPK signaling in CRC cells. AMPKα1 dominant negative mutation, shRNA-mediated knockdown or complete knockout (by CRISPR/Cas9 method) largely attenuated LB-100-induced AMPK activation and HCT-116 cytotoxicity. Notably, microRNA-17-92-mediated silence of PP2A (regulatory B subunit) also activated AMPK and induced HCT-116 cell death. Such effects were again largely attenuated by AMPKα mutation, silence or complete knockout. In vivo studies showed that intraperitoneal injection of LB-100 inhibited HCT-116 xenograft growth in nude mice. Its anti-tumor activity was largely compromised against HCT-116 tumors-derived from AMPKα1-knockout cells. We conclude that targeting PP2A by LB-100 and microRNA-17-92 activates AMPK signaling to inhibit CRC cells.

Targeting PP2A activates AMPK signaling to inhibit colorectal cancer cells

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Targeting PP2A activates AMPK signaling to inhibit colorectal cancer cells