Resistin causes G1 arrest in colon cancer cells through upregulation of <scp>SOCS</scp>3

Singh, Shweta; Chouhan, Surbhi; Mohammad, Naoshad; Bhat, Manoj Kumar

doi:10.1002/1873-3468.12655

Cited by 58 publications

(39 citation statements)

References 40 publications

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“…Not only is the adipokine resistin associated with obesity, inflammation, and various cancers [32,33,34], but high serum resistin levels have been implicated in the pathogenesis of cachexia in lung cancer [35], while resistin overexpression or upregulation is a feature of several human cancers, including oral cancer, renal cell carcinoma, chondrosarcoma and colon cancer [36,37,38,39]. Notably, resistin helps to promote tumor growth, drug resistance and metastasis in breast cancer [40,41,42].…”

Section: Discussionmentioning

confidence: 99%

Impacts of RETN genetic polymorphism on breast cancer development

et al. 2020

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The adipokine resistin is linked with obesity, inflammation and various cancers, including breast cancer. This study sought to determine whether certain polymorphisms in the gene encoding resistin, RETN, increase the risk of breast cancer susceptibility. We analyzed levels of resistin expression in breast cancer tissue and samples from The Cancer Genome Atlas database. We also examined associations between four RETN single nucleotide polymorphisms (SNPs; rs3745367, rs7408174, rs1862513 and rs3219175) and breast cancer susceptibility in 515 patients with breast cancer and 541 healthy women without cancer. Compared with wild-type (GG) carriers, those carrying the AG genotype of the RETN SNP rs3219175 and those carrying at least one A allele in the SNP rs3219175 had a higher chance of developing breast cancer (adjusted odds ratio, AOR: 1.295, 95% confidence intervals, CI: 1.065-1.575 and 2.202, 1.701-2.243, respectively). When clinical aspects and the RETN SNP rs7408174 were examined in the breast cancer cohort, the CT genotype was linked to late-stage disease, while women with luminal A disease and at least one C allele were likely to progress to stage III/IV disease and to develop highly pathological grade III disease. Moreover, resistin-positive individuals were at greater risk than resistin-negative individuals for developing pathological grade III disease (OR: 5.020; 95% CI: 1.380-18.259). This study details risk associations between resistin and RETN SNPs in breast cancer susceptibility in Chinese Han women.

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Section: Discussionmentioning

confidence: 99%

Impacts of RETN genetic polymorphism on breast cancer development

et al. 2020

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“…Sera from mice or lyophilized culture media from HepG2 cells treated with LG or HG were used to coat ELISA plates at 4 °C overnight. The plates were then processed as described previously [ 23 ]. Standard curves with different concentrations of recombinant hPCSK9 and mPCSK9 were prepared to quantify concentration of secretory PCSK9.…”

Section: Methodsmentioning

confidence: 99%

“…Total RNA from HepG2 cells and tissues was isolated with TRIzol™ (Invitrogen, CA, USA). Complementary DNA was prepared from 2 μg of total RNA as described previously [ 23 ]. Subsequently, RT-qPCR was performed using MESA GREEN SYBR MIX (Eurogentech, Belgium) with specific primer sets (Additional file 1 : Table S1).…”

Section: Methodsmentioning

confidence: 99%

Hepatocellular carcinoma-associated hypercholesterolemia: involvement of proprotein-convertase-subtilisin-kexin type-9 (PCSK9)

et al. 2018

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BackgroundPCSK9 regulates low-density lipoprotein cholesterol (LDLc) level and has been implicated in hypercholesterolemia. Aberrant plasma lipid profile is often associated with various cancers. Clinically, the relationship between altered serum lipid level and hepatocellular carcinoma (HCC) has been documented; however, the underlying cause and implications of such dyslipidemia remain unclear.MethodsThe present study includes the use of HepG2 tumor xenograft model to study the potential role of glucose (by providing 15% glucose via drinking water) in regulating PCSK9 expression and associated hypercholesterolemia. To support in vivo findings, in vitro approaches were used by incubating HCC cells in culture medium with different glucose concentrations or treating the cells with glucose uptake inhibitors. Impact of hypercholesterolemia on chemotherapy was demonstrated by exogenously providing LDLc followed by appropriate in vitro assays.ResultsWe observed that serum and hepatic PCSK9 level is decreased in mice which were provided with glucose containing water. Interestingly, serum and tumor PCSK9 level was upregulated in HepG2-tumor-bearing mice having access to water containing glucose. Additionally, elevated LDLc is detected in sera of these mice. In vitro studies indicated that PCSK9 expression was increased by high glucose availability with potential involvement of reactive oxygen species (ROS) and sterol regulatory element binding protein-1 (SREBP-1). Furthermore, it is also demonstrated that pre-treatment of cells with LDLc diminishes cytotoxicity of sorafenib in HCC cells.ConclusionTaken together, these results suggest a regulation of PCSK9 by high glucose which could contribute, at least partly, towards understanding the cause of hypercholesterolemia in HCC and its accompanied upshots in terms of altered response of HCC cells towards cancer therapy.Electronic supplementary materialThe online version of this article (10.1186/s40170-018-0187-2) contains supplementary material, which is available to authorized users.

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“…Author details 1 The Seventh A liated Hospital of Sun Yat-sen University, Shenzhen, China; 2 Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China; 3 Department of General Surgery, The Second A liated Hospital of Nanchang University, Nanchang, China; 4 Jiangxi Medical College of Nanchang University, Nanchang, China; 5 Jiangxi Province Key Laboratory of Molecular Medicine, Nanchang, China; 6 Otolaryngology Head and Neck Surgery, The Second A liated Hospital of Nanchang University, Nanchang, China. Table 3 The sequences for RT-qPCR…”

Section: Author's Contributionmentioning

confidence: 99%

“…In terms of clinical treatment, high rates of metastasis, cancer recurrence, and chemoresistance, make CRC challenging to treat at any stage. As previous studies have described that resistin exposure can block cells in the G1 phase, thereby prolonging their resistance and delaying the progression of p53 nonfunctional colon cancer cells [3]. In the eld of molecular targeted therapy, anti-epidermal growth factor receptor monoclonal antibodies, such as cetuximab or panitumumab, combined with chemotherapy have made some progress for the treatment of patients with RAS and BRAF wild-type metastatic CRC [4].…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA RP11-757G1.5 sponges miR-139-5p and upregulates YAP1 thereby promoting the proliferation and liver, spleen metastasis of colorectal cancer

Zhu

Tan

et al. 2020

Preprint

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Background: Accumulating evidence indicates that long non-coding RNAs (lncRNAs) acting as crucial regulators in tumorigenesis. However, its biological functions of lncRNAs in colorectal cancer (CRC) have not been systematically clarified. Methods: An unbiased screening was performed to identify disregulated lncRNAs revealed to be implicated in CRC carcinogenesis according to an online-available data dataset. In situ hybridization (ISH), RT-qPCR and RNA fluorescence in situ hybridization (RNA-FISH) were applied to detect RP11-757G1.5 expression in CRC tissues and cell lines. The associations of RP11-757G1.5 with clinicopathological characteristics were analyzed. Their effects on prognosis were analyzed by the Kaplan-Meier analysis, Log-rank test, Univariate and Multivariate Cox regression analysis. The potential biological function of RP11-757G1.5 in CRC was investigated by Colony formation, Edu cell proliferation, Flow cytometry, Wound healing and Transwell assays. Bioinformatics binding site analysis, Luciferase reporter assay, Ago2 immunoprecipitation assays, RNA pull-down assay, RT-qPCR and Western blotting were utilized to demonstrate the mechanism of RP11-757G1.5 acts as a molecular sponge of miR-139-5p to regulate the expression of YAP1. Finally, we further explore the potential role of RP11-757G1.5 in CRC orthotopic xenografts in vivio . Results: We discovered a novel oncogenic lncRNA RP11-757G1.5, that was overexpressed in CRC tissues, especially in aggressive cases. Moreover, up-regulation of RP11-757G1.5 strongly correlated with poor clinical outcomes of patients with CRC. Functional analyses revealed that RP11-757G1.5 promoted cell proliferation in vitro and in vivo . Furthermore, RP11-757G1.5 stimulated cell migration and invasion in vitro and in vivo . Mechanistic studies illustrated that RP11-757G1.5 regulated the expression of YAP1 through sponging miR-139-5p and inhibiting its activity thereby promoting CRC progression and development. Conclusions: Altogether, these results reveal a novel RP11-757G1.5/miR-139-5p/YAP1 regulatory axis that participates in CRC carcinogenesis and progression.

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Resistin causes G1 arrest in colon cancer cells through upregulation of SOCS3

Cited by 58 publications

References 40 publications

Impacts of RETN genetic polymorphism on breast cancer development

Impacts of RETN genetic polymorphism on breast cancer development

Hepatocellular carcinoma-associated hypercholesterolemia: involvement of proprotein-convertase-subtilisin-kexin type-9 (PCSK9)

Long noncoding RNA RP11-757G1.5 sponges miR-139-5p and upregulates YAP1 thereby promoting the proliferation and liver, spleen metastasis of colorectal cancer

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