scholarly journals Long noncoding RNA PICSAR/miR‐588/EIF6 axis regulates tumorigenesis of hepatocellular carcinoma by activating PI3K/AKT/mTOR signaling pathway

2020 ◽  
Vol 111 (11) ◽  
pp. 4118-4128 ◽  
Author(s):  
Zhikui Liu ◽  
Huanye Mo ◽  
Liankang Sun ◽  
Liang Wang ◽  
Tianxiang Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway

scholarly journals HULC long noncoding RNA silencing suppresses angiogenesis by regulating ESM-1 via the PI3K/Akt/mTOR signaling pathway in human gliomas

Oncotarget ◽  
2016 ◽  
Vol 7 (12) ◽  
pp. 14429-14440 ◽  
Author(s):  
Yu Zhu ◽  
Xuebin Zhang ◽  
Lisha Qi ◽  
Ying Cai ◽  
Ping Yang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Long Noncoding Rna ◽  
Rna Silencing ◽  
Noncoding Rna ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Human Gliomas

scholarly journals LINC00152 promotes proliferation in hepatocellular carcinoma by targeting EpCAM via the mTOR signaling pathway

Oncotarget ◽  
2015 ◽  
Vol 6 (40) ◽  
pp. 42813-42824 ◽  
Author(s):  
Jie Ji ◽  
Junwei Tang ◽  
Lei Deng ◽  
Yu Xie ◽  
Runqiu Jiang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway

scholarly journals SB365 inhibits angiogenesis and induces apoptosis of hepatocellular carcinoma through modulation of PI3K/Akt/mTOR signaling pathway

2012 ◽  
Vol 103 (11) ◽  
pp. 1929-1937 ◽  
Author(s):  
Sang-Won Hong ◽  
Kyung Hee Jung ◽  
Hee-Seung Lee ◽  
Myung-Joo Choi ◽  
Mi Kwon Son ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway

scholarly journals Emerging Role of mTOR Signaling-Related miRNAs in Cardiovascular Diseases

2018 ◽  
Vol 2018 ◽  
pp. 1-23 ◽  
Author(s):  
Arun Samidurai ◽  
Rakesh C. Kukreja ◽  
Anindita Das
Keyword(s):  
Cardiovascular Diseases ◽  
Cardiovascular System ◽  
Signaling Pathway ◽  
Noncoding Rna ◽  
Current Knowledge ◽  
Mammalian Target Of Rapamycin ◽  
Vital Role ◽  
Mtor Signaling ◽  
Cellular Growth ◽  
Mtor Signaling Pathway

Mechanistic/mammalian target of rapamycin (mTOR), an atypical serine/threonine kinase of the phosphoinositide 3-kinase- (PI3K-) related kinase family, elicits a vital role in diverse cellular processes, including cellular growth, proliferation, survival, protein synthesis, autophagy, and metabolism. In the cardiovascular system, the mTOR signaling pathway integrates both intracellular and extracellular signals and serves as a central regulator of both physiological and pathological processes. MicroRNAs (miRs), a class of short noncoding RNA, are an emerging intricate posttranscriptional modulator of critical gene expression for the development and maintenance of homeostasis across a wide array of tissues, including the cardiovascular system. Over the last decade, numerous studies have revealed an interplay between miRNAs and the mTOR signaling circuit in the different cardiovascular pathophysiology, like myocardial infarction, hypertrophy, fibrosis, heart failure, arrhythmia, inflammation, and atherosclerosis. In this review, we provide a comprehensive state of the current knowledge regarding the mechanisms of interactions between the mTOR signaling pathway and miRs. We have also highlighted the latest advances on mTOR-targeted therapy in clinical trials and the new perspective therapeutic strategies with mTOR-targeting miRs in cardiovascular diseases.

scholarly journals Interferon-Induced Transmembrane Protein 3 Expression Upregulation Is Involved in Progression of Hepatocellular Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Yuli Hou ◽  
Shanshan Wang ◽  
Mengdan Gao ◽  
Jing Chang ◽  
Jianping Sun ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Transmembrane Protein ◽  
Metastatic Potential ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Purpose. Interferon-induced transmembrane protein 3 (IFITM3) is a key signaling molecule regulating cell growth in some tumors, but its function and mechanism in hepatocellular carcinoma (HCC) remain unknown. Our study investigated the relationship between the expression of IFITM3 and HCC development. Material and Methods. IFITM3 expression was identified via multiple gene expression databases and investigated in HCC tissue samples. Then, PLC/PRF/5 cells were transfected with lentivirus to knock down and overexpress the expression of IFITM3. IFITM3 expression, cell proliferation, and migration were detected by qRT-PCR, western blotting, QuantiGene Plex 2.0 assay, immunohistochemistry, CCK-8, and wound healing tests. RNA-seq technology identified the PI3K/AKT/mTOR pathway as an IFITM3-related signaling pathway for investigation. Results. IFITM3 expression was higher in HCC tissues than in adjacent normal tissues, and the level of IFITM3 was higher in HCC tissues with low differentiation and metastatic potential than in those with high/medium differentiation and without metastatic potential. A higher RNA level of IFITM3 was found in samples with IFITM3 rs12252-CC genotype rather than the TT genotype. Knockdown of IFITM3 in PLC/PRF/5 cells inhibited cell proliferation and migration, blocked the expression of the PI3K/AKT/mTOR signaling pathway, and decreased the expression of vimentin. The results were opposite with the overexpression of IFITM3. Conclusion. Upregulation of IFITM3 plays a role in the development of HCC. Possibly through regulating HCC cell proliferation and migration, these effects are associated with the PI3K/AKT/mTOR signaling pathway. Upregulation of IFITM3 is also associated with the IFITM3 rs12252-CC genotype.

Oxaliplatin and Gedatolisib (PKI-587) Co-Loaded Hollow Polydopamine Nano-Shells with Simultaneous Upstream and Downstream Action to Re-Sensitize Drugs-Resistant Hepatocellular Carcinoma to Chemotherapy

2021 ◽  
Vol 17 (1) ◽  
pp. 18-36
Author(s):  
Yin-Ci Zhang ◽  
Cheng-Guang Wu ◽  
A-Min Li ◽  
Yong Liang ◽  
Dong Ma ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Dna Damage ◽  
Drug Resistance ◽  
Combination Therapy ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Repair Pathway ◽  
Mtor Signaling Pathway ◽  
Damage Repair ◽  
Anti Cancer

Multidrug resistance (MDR) is a key to the ineffectiveness of hepatocellular carcinoma (HCC) chemotherapy. Oxaliplatin (OXA), as one of the first-line chemotherapeutic drugs for HCC, abnormally activates the PI3K/AKT/mTOR signaling pathway and DNA damage repair pathway (NHEJ and HR), causing drug resistance and consequnet compromised efficacy. Herein, we developed a hollow polydopamine nanoparticle (H-PDA)-based nano-delivery system (O/P-HP) that contained OXA and a dual PI3K/mTOR inhibitor PKI-587 with complementary effects for combating drug resistance in cancer chemotherapy. The hollow structure of H-PDA endowed O/P-HP with high loading efficiencies of OXA and PKI-587–up to 49.6% and 7.0%, respectively. In addition, benefiting from the intracellular delivery of H-PDA as well as the highly concentrated drugs therein, O/P-HP inhibited the proliferation of OXA-resistant HR cells, resulting in a cell viability of only 17.63%. These values were significantly superior to those with OXA single-agent treatment and treatment with free OXA in combination with PKI-587. We examined the intrinsic mechanisms of the combination therapy: O/PHP had excellent anti-cancer effects via the simultaneous upstream and downstream action to re-sensitize HR cells to chemotherapy; OXA induced strong apoptosis via the direct platinum lesions on DNA molecules, while PKI-587 normalized the abnormally activated PI3K/AKT/mTOR signaling pathway and DNA damage repair pathway (NHEJ and HR) that could attenuate the effectiveness of OXA, thus resulting in inhibition of cell proliferation, migration and DNA repair enzyme activity and the augment of apoptotic effects. Such combination therapy, with simultaneous upstream and downstream action, may be a strategy for minimizing resistance for anti-cancer treatments.

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