Long non-coding RNA CASC2 inhibits breast cancer cell growth and metastasis through the regulation of the miR-96-5p/SYVN1 pathway

Ze-jun, Gao; Wang, Hai; Li, Hangyu; Li, Min; Wang, Jia; Zhang, Wenwen; Su, Dongming; Tang, Jinhai

doi:10.3892/ijo.2018.4522

Cited by 26 publications

(23 citation statements)

References 29 publications

(46 reference statements)

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“…[ 36 ] CASC2 inhibited breast cancer cell growth and metastasis through the regulation of the miR‐96‐5p/SYVN1 pathway. [ 37 ] Upregulation of CASC2 sensitized glioma to temozolomide cytotoxicity through autophagy inhibition by sponging miR‐193a‐5p and regulating mTOR expression. [ 38 ] Especially, CASC2 upregulated PTEN to suppress proliferation and metastasis of pancreatic cancer cells by downregulating miR‐21 and Akt signaling.…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg3 suppresses the growth of gemcitabine‐resistant pancreatic cancer cells by upregulating lncRNA‐CASC2 and activating PTEN signaling

Zou¹,

Zou

et al. 2020

J Biochem & Molecular Tox

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Pancreatic cancer is one of the most fatal malignancies with high mortality. Gemcitabine (GEM)‐based chemotherapy is the most important treatment. However, the development of GEM resistance leads to chemotherapy failure. Previous studies demonstrated the anticancer activity of ginsenoside Rg3 in a variety of carcinomas through modulating multiple signaling pathways. In the present study, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide assay, colony formation assay, flow cytometry apoptosis assay, Western blotting assay, xenograft experiment, and immunohistochemistry assay were performed in GEM‐resistant pancreatic cancer cell lines. Ginsenoside Rg3 inhibited the viability of GEM‐resistant pancreatic cancer cells in a time‐dependent and concentration‐dependent manner through induction of apoptosis. The level of long noncoding RNA cancer susceptibility candidate 2 (CASC2) and PTEN expression was upregulated by the ginsenoside Rg3 treatment, and CASC2/PTEN signaling was involved in the ginsenoside Rg3‐induced cell growth suppression and apoptosis in GEM‐resistant pancreatic cancer cells. Ginsenoside Rg3 could be an effective anticancer agent for chemoresistant pancreatic cancer.

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Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg3 suppresses the growth of gemcitabine‐resistant pancreatic cancer cells by upregulating lncRNA‐CASC2 and activating PTEN signaling

Zou¹,

Zou

et al. 2020

J Biochem & Molecular Tox

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“…In this study, HRD1 inhibited aerobic glycolysis in breast cancer cells, providing new evidence for a role as a regulator of tumor metabolism. Our previous studies had revealed that HRD1 had a tumor suppressive effect that involved suppression of breast cancer cell proliferation, migration and invasion [17][18][19].…”

Section: Discussionmentioning

confidence: 99%

HRD1 Elicitation of An Anti-Warburg Effect by Targeting PFKP to Inhibit Breast Cancer Growth and Progression

Fan

Wang

et al. 2020

Preprint

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Background: Our previous studies have shown that the E3 ubiquitin ligase of HMG-CoA reductase degradation 1 (HRD1) functions as a tumor suppressor, as overexpression of HRD1 suppressed breast cancer proliferation and invasion. However, its role in breast cancer cell glucose metabolism was unclear. Here, our aim was to uncover the role and molecular mechanisms of HRD1 in regulating aerobic glycolysis in breast cancer. Methods: The effect of HRD1 on robic glycolysis in breast cancer cells were assessed. Then the proliferation, colony formation ability, invasion and migration of breast cancer cells were evaluated. The relationship between HRD1 and PFKP was validated by Mass spectrometry analysis, immunofluorescence and co-immunoprecipitation. The level of PFKP ubiquitination was measured using ubiquitylation assay. Furthermore, the tumor growth in vivo were observed by subcutaneous tumorigenesis in nude mice. Results: We found that upregulation of HRD1 clearly decreased aerobic glycolysis, and subsequently inhibited breast cancer proliferation and invasion. Mass spectrometry analysis results revealed a large HRD1 interactome, which included PFKP (platelet isoform of phosphofructokinase), a critical enzyme involved in the Warburg Effect in breast cancer. Mechanistically, HRD1 interacted and colocalized with PFKP in the cytoplasm, targeted PFKP for ubiquitination and degradation, and ultimately reduced PFKP expression and activity in breast cancer cells. Conclusions: Our findings reveal a new regulatory role of HRD1 in Warburg effect and provide a key contributor in breast cancer metabolism.

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“…Induction of ER stress leads to upregulation of several genes such as WARS (tryptophanyl-tRNA synthetase), HERP (homocysteine-inducible ER protein with ubiquitin like domain 1), DNAJC3 (also called P58IPK), ER degradation-enhancing alpha-mannosidase-like 1 (EDEM1) and leads to caspase activation, release of mitochondrial intermembrane proteins and dissipation of mitochondrial transmembrane potential (ΔΨm) [53]. Synovial apoptosis inhibitor 1 (SYVN1), an ER-associated degradation (ERAD) E3 ubiquitin ligase, could inhibit the breast cancer cell growth and metastasis through the miR-96-5p/SYVN1 axis [54]. Site 1 protease (S1P), SREBP cleavage-activating protein (SCAP) and acetyl-CoA acetyltransferase 1 (ACAT1) were involved in the lipid metabolism [55].…”

Section: Discussionmentioning

confidence: 99%

Psoralen inhibits malignant proliferation and induces apoptosis through triggering endoplasmic reticulum stress in human SMMC7721 hepatoma cells

et al. 2019

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Background: Psoralen is a coumarin-like and coumarin-related benzofuran glycoside, which is a commonly used traditional Chinese medicine to treat patients with kidney and spleen-yang deficiency symptom. Psoralen has been reported to show estrogen-like activity, antioxidant activity, osteoblastic proliferation accelerating activity, antitumor effects and antibacterial activity. However, the antitumor mechanism of psoralen is not fully understood. This study aimed to investigate the therapeutic efficacy of psoralen in human hepatoma cell line SMMC7721 and the mechanism of antitumor effects. Results: Psoralen inhibited proliferation of SMMC7721 in a dose-and time-dependent manner, and promoted apoptosis. Further, psoralen activated the ER stress signal pathway, including the expansion of endoplasmic reticulum, increasing the mRNA levels of GRP78, DDIT3, ATF4, XBP1, GADD34 and the protein levels of GDF15, GRP78, IRE1α, XBP-1s in a time-dependent manner. Psoralen induces cell cycle arrest at G1 phase by enhancing CyclinD1 and reducing CyclinE1 expression. Moreover, TUDC couldn't inhibit the psoralen-induced ER stress in SMMC7721 cells. Conclusions: Psoralen can inhibit the proliferation of SMMC7721 cells and induce ER stress response to induce cell apoptosis, suggesting that psoralen may represent a novel therapeutic option for the prevention and treatment hepatocellular carcinoma.

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Long non-coding RNA CASC2 inhibits breast cancer cell growth and metastasis through the regulation of the miR-96-5p/SYVN1 pathway

Cited by 26 publications

References 29 publications

Ginsenoside Rg3 suppresses the growth of gemcitabine‐resistant pancreatic cancer cells by upregulating lncRNA‐CASC2 and activating PTEN signaling

Ginsenoside Rg3 suppresses the growth of gemcitabine‐resistant pancreatic cancer cells by upregulating lncRNA‐CASC2 and activating PTEN signaling

HRD1 Elicitation of An Anti-Warburg Effect by Targeting PFKP to Inhibit Breast Cancer Growth and Progression

Psoralen inhibits malignant proliferation and induces apoptosis through triggering endoplasmic reticulum stress in human SMMC7721 hepatoma cells

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