Long non-coding RNA HAGLROS regulates lipid metabolism reprogramming in intrahepatic cholangiocarcinoma via the mTOR signaling pathway

2020 ◽  
Vol 115 ◽  
pp. 104466 ◽  
Author(s):  
Jun Ma ◽  
Jinfeng Feng ◽  
Xiang Zhou
Keyword(s):  
Lipid Metabolism ◽  
Signaling Pathway ◽  
Intrahepatic Cholangiocarcinoma ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Silencing long non-coding RNA ROR improves sensitivity of non-small-cell lung cancer to cisplatin resistance by inhibiting PI3K/Akt/mTOR signaling pathway

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831769756 ◽  
Author(s):  
Hui Shi ◽  
Jin Pu ◽  
Xiao-Li Zhou ◽  
Yun-Ye Ning ◽  
Chong Bai
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Negative Control ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Control Groups ◽  
Over Expression ◽  
Non Coding Rna ◽  
Protein Expressions ◽  
Long Non Coding Rna

This study aimed to investigate the effects of long non-coding RNA ROR (regulator of reprogramming) on cisplatin (DDP) resistance in patients with non-small-cell lung cancer by regulating PI3K/Akt/mTOR signaling pathway. Human cisplatin-resistant A549/DDP cell lines were selected and divided into control group, negative control group, si-ROR group, ROR over-expression group, Wortmannin group, and ROR over-expression + Wortmannin group. MTT assay was used to determine the optimum inhibitory concentration of DDP. Quantitative real-time polymerase chain reaction and western blotting were applied to detect expressions of long non-coding RNA ROR, PI3K, Akt, and mTOR. Colony-forming assay, scratch test, Transwell assay, and flow cytometry were conducted to detect cell proliferation, migration, invasion, and apoptosis, respectively. Tumor-formation assay was performed to detect the growth of transplanted tumors. Long non-coding RNA ROR expression was high in human A549/DDP cell lines. Compared with the control and negative control groups, the mRNA and protein expressions of PI3K, Akt, mTOR, and bcl-2 decreased, whereas the mRNA and protein expression of bax and the sensitivity of cells to DDP significantly increased. Cell proliferation, migration, and invasion abilities decreased in the si-ROR and Wortmannin groups. In comparison with control and negative control groups, the mRNA and protein expressions of PI3K, Akt, mTOR, and bcl-2 increased, whereas the mRNA and protein expressions of bax decreased, the sensitivity of cells to DDP significantly increased, and cell proliferation, migration, and invasion abilities decreased in the ROR over-expression group. For nude mice in tumor-formation assay, compared with control and negative control groups, the tumor weight was found to be lighter (1.03 ± 0.15) g, the protein expressions of PI3K, Akt, mTOR, and bcl-2 decreased, and the protein expression of bax increased in the si-ROR group. Long non-coding RNA ROR may affect the sensitivity of lung adenocarcinoma cells to DDP by targeting PI3K/Akt/mTOR signaling pathway.

Long non-coding RNA tumor protein 53 target gene 1 promotes cervical cancer development via regulating microRNA-33a-5p to target forkhead box K2 (Preprint)

2021 ◽  
Author(s):  
Yanyan Liu Sr ◽  
xiaomei Liu ◽  
xiuying Yuan ◽  
poling Feng ◽  
zhiwei Ouyang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Signaling Pathway ◽  
Target Gene ◽  
Mtor Signaling ◽  
Regulatory Function ◽  
Clinical Samples ◽  
Mtor Signaling Pathway ◽  
Forkhead Box ◽  
Non Coding Rna ◽  
Long Non Coding Rna

BACKGROUND Long non-coding RNA tumor protein 53 target gene 1 (TP53TG1) has been studied in multiple diseases, while the regulatory function of TP53TG1 on cervical cancer (CC) via regulating microRNA (miR)-33a-5p to target Forkhead box K2 (FOXK2) remains limited. This study aims to unearth the effects of TP53TG1/miR-33a-5p/FOXK2 axis on CC. OBJECTIVE This study aims to unearth the effects of TP53TG1/miR-33a-5p/FOXK2 axis on CC. METHODS The clinical samples were collected and TP53TG1, miR-33a-5p and FOXK2 levels were examined in CC tissues. The CC cells were transfected with high- or low-expressed TP53TG1, FOXK2 and miR-33a-5p to determine the change of CC cell biological activities and the status of phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. The tumorigenesis in nude mice was conducted. The relationship among TP53TG1, miR-33a-5p and FOXK2 was validated. RESULTS TP53TG1 and FOXK2 were enriched and miR-33a-5p was inhibited in CC. The reduced TP53TG1 or FOXK2 or elevated miR-33a-5p decelerated the CC cell development and the activation of PI3K/AKT/mTOR signaling pathway. The depleted FOXK2 or enriched miR-33a-5p reversed the effects of decreased TP53TG1. TP53TG1 sponged miR-33a-5p which targeted FOXK2. The experiment in vivo validated the outcomes of the experiment in vitro. CONCLUSIONS TP53TG1 accelerates the CC development via regulating miR-33a-5p to target FOXK2 with the involvement of PI3K/AKT/mTOR signaling pathway. This study provides novel theory references and a distinct direction for the therapy strategies of CC.

scholarly journals Long non-coding RNA CRNDE promote the progression of tongue squamous cell carcinoma through regulating the PI3K/AKT/mTOR signaling pathway

RSC Advances ◽  
2019 ◽  
Vol 9 (37) ◽  
pp. 21381-21390
Author(s):  
Zhongheng Yang ◽  
Weizhi Chen
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Colorectal Neoplasia ◽  
Tongue Squamous Cell Carcinoma ◽  
Mtor Signaling Pathway ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Long non-coding RNAs (lnRNAs) colorectal neoplasia differentially expressed (CRNDE) has been identified as a crucial regulator involved in tongue squamous cell carcinoma (TSCC).

scholarly journals Glucose-induced lipid deposition in goose primary hepatocytes is dependent on the PI3K-Akt-mTOR signaling pathway

2016 ◽  
Vol 68 (4) ◽  
pp. 853-861
Author(s):  
Chunchun Han ◽  
Shouhai We ◽  
Fang He ◽  
Song Qi ◽  
Xiangping Xiong ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Signaling Pathway ◽  
Fatty Acid Oxidation ◽  
Mtor Pathway ◽  
Mtor Signaling ◽  
Acid Oxidation ◽  
Lipid Deposition ◽  
Mtor Signaling Pathway ◽  
Primary Hepatocytes

Previously we showed that fatty liver formation in overfed geese was accompanied by PI3K-Akt-mTOR pathway activation and changes in plasma glucose concentrations. Here, we show that glucose acts in goose hepatocellular lipid metabolism through the PI3K-Akt-mTOR signaling pathway. We observed that glucose increased lipogenesis, decreased fatty acid oxidation and increased very low density lipoprotein triglyceride (VLDL-TG) assembly and secretion. Co-treatment with glucose and inhibitors of the PI3K-Akt-mTOR pathway (LY294002, rapamycin, NVP-BEZ235) decreased the levels of factors involved in lipogenesis and increased the levels of factors involved in fatty acid oxidation and VLDL-TG assembly and secretion. These findings show that inhibition of the PI3K-Akt-mTOR pathway decreased glucose-induced lipogenesis, inhibited the downregulation of fatty acid oxidation by glucose and increased the upregulation of VLDL-TG assembly and secretion by glucose. The results presented herein provide further support for the role of the PI3K-Akt-mTOR pathway in lipid metabolism as we showed that in goose primary hepatocytes, glucose acts through the PI3K-Akt-mTOR-dependent pathway to stimulate lipid deposition by increasing lipogenesis and decreasing fatty acid oxidation and VLDL-TG assembly and secretion.

scholarly journals Apolipoprotein C-II induces EMT to Promote Gastric Cancer Peritoneal Metastasis via PI3K/AKT/mTOR Pathway

2021 ◽  
Author(s):  
Chao Wang ◽  
Zhi Yang ◽  
En Xu ◽  
Xingzhou Wang ◽  
Zijian Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Lipid Metabolism ◽  
Signaling Pathway ◽  
Peritoneal Metastasis ◽  
Mtor Signaling ◽  
Tandem Mass ◽  
Mtor Signaling Pathway ◽  
Apolipoprotein C

Abstract Background: Peritoneal metastasis (PM) occurs frequently in patients with gastric cancer (GC) and confers poor survival. Lipid metabolism and epithelial-mesenchymal transition (EMT) play an important role in GC metastasis. As Apolipoprotein C-II (APOC2) is a key protein in lipid metabolism, few studies have investigated the role of APOC2 in PM. This study aims to elucidate the potential molecular mechanism of APOC2 in the PM of GC.Methods: The Tandem Mass Tagging (TMT) method followed by liquid chromatography-tandem mass spectrometry-based proteomics analysis was used to compare the levels of differentially expressed proteins between human PM and GC tissues. APOC2 expression was evaluated by immunoblotting, and immunohistochemistry analysis (n = 111). APOC2 over-expression and knock-down expression cell models were developed and tested in vitro. RNA sequencing analysis evaluated the changes in gene expression after APOC2 knockdown in GC cells. The Agilent Seahorse XF platform and lipid staining assay were used to evaluate the role of APOC2 in lipid metabolism of GC cells. Spheroid cell invasion assay, apoptosis assay, colony formation assay, wound-healing assays, and transwell assays were performed and peritoneal implants into nude mice were done to assess the biological effects of APOC2. The underlying mechanisms were investigated using Western blot, inhibitor or activator treatment assays.Results: APOC2 was highly abundant in GC cells and PM tissues. And high APOC2 levels in GC tissues correlated with poor patient prognosis. Knockdown of APOC2 inhibited the malignant phenotype of cancer cells and EMT significantly. Massive gene expression alterations after APOC2 knockdown, which were associated with various signaling pathways, especially the PI3K/AKT signaling pathway and lipid metabolism. Furthermore, the regulatory effects of APOC2 on the EMT were partially attributed to the PI3K/AKT/mTOR signaling pathway. The results in vivo also showed that APOC2 modulated GC PM.Conclusions: We verified that knockdown of APOC2 suppressed GC cell Lipid metabolism, proliferation, migration, invasion, and EMT, accompanied by inactivation of PI3K/AKT/mTOR signaling pathway. APOC2 overexpression had the opposite effects GC cell phenotypes and mechanisms. Collectively, our results identified APOC2 in PM as a potential therapeutic target.

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