Downregulation of LINC00958 inhibits proliferation, invasion and migration, and promotes apoptosis of colorectal cancer cells by targeting miR‑3619‑5p

Sun, Ye; Liu, Yi; Cai, Yun; Han, Pingping; Wang, Rui; Cao, Liu; He, Shuixiang

doi:10.3892/or.2020.7707

Cited by 11 publications

(10 citation statements)

References 33 publications

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“…In addition, Brownmiller et al found a significant difference in the expression of the Y chromosome lncRNA linc-SPRY3-2/3/4 between radiation-sensitive and radiation-resistant non-small cell lung cancer cells, and confirmed that knockdown of linc-SPRY3-2/3/4 promoted cell viability and resistance to apoptosis after treatment with 8 Gy [28]. In this study, we found that LINC00958 was upregulated in colorectal cancer tissues, which was in accordance with a previous study [29]. Further analysis showed that a high level of LINC00958 was positively correlated with T stage and predicted poor overall survival and disease-free survival.…”

Section: Discussionsupporting

confidence: 92%

Long noncoding RNA LINC00958 suppresses apoptosis and radiosensitivity of colorectal cancer through targeting miR-422a

et al. 2021

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Background Long noncoding RNAs (lncRNAs) have been elucidated to participate in the development and progression of various cancers. In this study, we aimed to explore the underlying functions and mechanisms of LINC00958 in colorectal cancer. Methods LINC00958 expression in colorectal cancer tissues was examined by qRT-PCR. The correlations between LINC00958 expression and clinical characteristics and prognosis were evaluated. The biological functions of LINC00958 were detected by CCK-8, MTT, colony formation and flow cytometric analyses. RNA pulldown, RIP and luciferase reporter assays were used to confirm the regulatory effects of LINC00958 on miR-422a. Rescue experiments were performed to detect the effects of miR-422a on the roles of LINC00958. Results LINC00958 was upregulated in colorectal cancer tissues and cell lines. High LINC00958 levels were positively associated with T stage and predicted poor prognosis. Cell experiments showed that LINC00958 promoted cell proliferation and suppressed apoptosis and sensitivity to radiotherapy in vitro and promoted tumor growth in vivo. Bioinformatics analysis predicted the binding site of miR-422a on LINC00958. Mechanistically, RNA pulldown, RIP and luciferase reporter assays demonstrated that LINC00958 specifically targeted miR-422a. In addition, we found that miR-422a suppressed MAPK1 expression by directly binding to the 3’-UTR of MAPK1, thereby inhibiting cell proliferation and enhancing cell apoptosis and radiosensitivity. Furthermore, miR-422a rescued the roles of LINC00958 in promoting MAPK1 expression and cell proliferation and decreasing cell apoptosis and radiosensitivity. Conclusions LINC00958 promoted MAPK1 expression and cell proliferation and suppressed cell apoptosis and radiosensitivity by targeting miR-422a, which suggests that it is a potential biomarker for the prognosis and treatment of colorectal cancer.

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Section: Discussionsupporting

confidence: 92%

Long noncoding RNA LINC00958 suppresses apoptosis and radiosensitivity of colorectal cancer through targeting miR-422a

et al. 2021

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“…We screened our RNA-seq data analyzed by NONCODE database [ 18 ] obtained from clinical specimens of normal ovarian tissues ( n = 6) and ovarian cancers ( n = 15) [ 15 , 16 ]. Screening NONCODE v4 transcripts abundantly expressed in ovarian cancer compared with normal ovarian tissues by ≥10-folds at an FDR q -value threshold <0.05, we identified 10 particular lincRNAs ( Table 1 ), including known oncogenic RNAs: competing endogenous lncRNA 2 for microRNA let-7b ( CERNA2 )/ human ovarian cancer-specific transcript 2 (HOST2) [ 19 ], urothelial cancer associated 1 ( UCA1 ) [ 14 , 20 , 21 , 22 ], and long intergenic non-protein coding RNA 958 (LINC00958) [ 23 ]. CERNA2 / HOST2 was shown to promote ovarian cancer cell proliferation, partly by sponging the tumor suppressor let-7b [ 19 ].…”

Section: Resultsmentioning

confidence: 99%

Long Intergenic Noncoding RNA OIN1 Promotes Ovarian Cancer Growth by Modulating Apoptosis-Related Gene Expression

Takeiwa

Mitobe

Ikeda

et al. 2021

IJMS

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Patients with advanced ovarian cancer usually exhibit high mortality rates, thus more efficient therapeutic strategies are expected to be developed. Recent transcriptomic studies revealed that long intergenic noncoding RNAs (lincRNAs) can be a new class of molecular targets for cancer management, because lincRNAs likely exert tissue-specific activities compared with protein-coding genes or other noncoding RNAs. We here show that an unannotated lincRNA originated from chromosome 10q21 and designated as ovarian cancer long intergenic noncoding RNA 1 (OIN1), is often overexpressed in ovarian cancer tissues compared with normal ovaries as analyzed by RNA sequencing. OIN1 silencing by specific siRNAs significantly exerted proliferation inhibition and enhanced apoptosis in ovarian cancer cells. Notably, RNA sequencing showed that OIN1 expression was negatively correlated with the expression of apoptosis-related genes ras association domain family member 5 (RASSF5) and adenosine A1 receptor (ADORA1), which were upregulated by OIN1 knockdown in ovarian cancer cells. OIN1-specifc siRNA injection was effective to suppress in vivo tumor growth of ovarian cancer cells inoculated in immunodeficient mice. Taken together, OIN1 could function as a tumor-promoting lincRNA in ovarian cancer through modulating apoptosis and will be a potential molecular target for ovarian cancer management.

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“…The primary characteristics of tumors are malignant proliferation and imbalance between cell proliferation and apoptosis [ 23 ]. Inhibiting proliferation and inducing apoptosis are excellent strategies for tumor treatment [ 24 ]. Previous research has shown that GLSP and G. lucidum triterpenes in G. lucidum spore powder can effectively inhibit tumors [ 25 , 26 ].…”

Section: Discussionmentioning

confidence: 99%

Ganoderma lucidum Spore Polysaccharide Inhibits the Growth of Hepatocellular Carcinoma Cells by Altering Macrophage Polarity and Induction of Apoptosis

Song

Li²,

Gu³

et al. 2021

Journal of Immunology Research

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Background. Ganoderma lucidum has certain components with known pharmacological effects, including strengthening immunity and anti-inflammatory activity. G. lucidum seeds inherit all its biological characteristics. G. lucidum spore polysaccharide (GLSP) is the main active ingredient to enhance these effects. However, its specific biological mechanisms are not exact. Our research is aimed at revealing the specific biological mechanism of GLSP to enhance immunity and inhibit the growth of H22 hepatocellular carcinoma cells. Methods. We extracted primary macrophages (Mø) from BALB/c mice and treated them with GLSP (800 μg/mL, 400 μg/mL, and 200 μg/mL) to observe its effects on macrophage polarization and cytokine secretion. We used GLSP and GLSP-intervened macrophage supernatant to treat H22 tumor cells and observed their effects using MTT and flow cytometry. Moreover, real-time fluorescent quantitative PCR and western blotting were used to observe the effect of GLSP-intervened macrophage supernatant on the PI3K/AKT and mitochondrial apoptosis pathways. Results. In this study, GLSP promoted the polarization of primary macrophages to M1 type and the upregulation of some cytokines such as TNF-α, IL-1β, IL-6, and TGF-β1. The MTT assay revealed that GLSP+Mø at 400 μg/mL and 800 μg/mL significantly inhibited H22 cell proliferation in a dose-dependent manner. Flow cytometry analysis revealed that GLSP+Mø induced apoptosis and cell cycle arrest at the G2/M phase, associated with the expression of critical genes and proteins (PI3K, p-AKT, BCL-2, BAX, and caspase-9) that regulate the PI3K/AKT pathway and apoptosis. GLSP reshapes the tumor microenvironment by activating macrophages, promotes the polarization of primary macrophages to M1 type, and promotes the secretion of various inflammatory factors and cytokines. Conclusion. Therefore, as a natural nutrient, GLSP is a potential agent in hepatocellular carcinoma cell treatment and induction of apoptosis.

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Downregulation of LINC00958 inhibits proliferation, invasion and migration, and promotes apoptosis of colorectal cancer cells by targeting miR‑3619‑5p

Cited by 11 publications

References 33 publications

Long noncoding RNA LINC00958 suppresses apoptosis and radiosensitivity of colorectal cancer through targeting miR-422a

Long noncoding RNA LINC00958 suppresses apoptosis and radiosensitivity of colorectal cancer through targeting miR-422a

Long Intergenic Noncoding RNA OIN1 Promotes Ovarian Cancer Growth by Modulating Apoptosis-Related Gene Expression

Ganoderma lucidum Spore Polysaccharide Inhibits the Growth of Hepatocellular Carcinoma Cells by Altering Macrophage Polarity and Induction of Apoptosis

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