Retracted Article: SNHG3 promotes proliferation and invasion by regulating the miR-101/ZEB1 axis in breast cancer

Chang, Liang; Hu, Zhuang; Zhou, Zhenyu; Zhang, Hui

doi:10.1039/c8ra02090f

Cited by 10 publications

(7 citation statements)

References 39 publications

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“…SNHG3 enhanced the malignant process of colorectal cancer 37. SNHG3 promoted proliferation and invasion in breast cancer38 and lung adenocarcinoma 39. In HCC, it was reported that SNHG3 was significantly upregulated and highly correlated with tumor size and relapse 40.…”

Section: Discussionmentioning

confidence: 98%

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<p>LncSNHG3/miR-139-5p/BMI1 axis regulates proliferation, migration, and invasion in hepatocellular carcinoma</p>

Wu¹,

Liu²,

Jin³

et al. 2019

OTT

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ObjectiveEmerging evidence has revealed that lncRNA small nucleolar RNA host gene 3 (SNHG3) is involved in cell proliferation, migration, and invasion in various tumors. However, the underlying molecular mechanism of SNHG3 in hepatocellular carcinoma (HCC) is still not fully explored.MethodsQuantitative reverse transcriptase PCR was employed to detect the expression of SNHG3, miR-139-5p, and BMI1. Colony assay and MTT assay were used to detect the proliferation. Transwell assay was introduced to measure the migration and invasion ability. Bioinformatics analysis and luciferase reporter assay were used to confirm the relationship between SNHG3, miR-139-5p, and BMI1. An animal experiment was adopted to detect the function of SNHG3 in vivo.ResultsSNHG3 and BMI1 were upregulated in HCC, while miR-139-5p was downregulated. Knockdown of SNHG3 or BMI1 and overexpression of miR-139-5p could inhibit cell proliferation, migration, and invasion in HCC. miR-139-5p was a target of SNHG3 and BMI1 was a direct target mRNA of miR-139-5p. Silencing SNHG3 could impair the tumor progression in vivo.ConclusionThe lncRNA SNHG3/miR-139-5p/BMI1 axis plays an important role in cell proliferation, migration, and invasion in HCC.

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Section: Discussionmentioning

confidence: 98%

“…We proposed that maybe the culture condition, knockdown efficiency, etc., were different in our two references, which led to distinct results. Besides, in other cancers such as breast cancer and lung cancer,38,39 SNHG3 knockdown inhibited cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

<p>LncSNHG3/miR-139-5p/BMI1 axis regulates proliferation, migration, and invasion in hepatocellular carcinoma</p>

Wu¹,

Liu²,

Jin³

et al. 2019

OTT

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“…The results indicated that knockdown of CAF-secreted exosomal the decrease of SNHG3 expression inhibited cell growth and glycolysis metabolism of breast tumor cells in vitro and in vivo. Accumulating studies suggested that small nucleolar RNA host genes (SNHGs) could function as endogenous RNAs (ceRNAs) to regulate cancer cells by sponging miRNA, such as miR-182-5p, miR-186-5p and miR-101 [12,27,28]. Therefore, we proposed whether CAF-secreted exosomal SNHG3 could regulate miRNA in cancer cells [18,28].…”

Section: Discussionmentioning

confidence: 99%

“…It was reported that SNHG3 was overexpressed in liver cancer, breast cancer, and colorectal cancer, which was associated with poor survival and prognosis in tumor-bearing patients [10,11,13,18,27]. Importantly, SNHG3 was identified as a potential oncogene in breast cancer based on previous studies which focused on cancer cell-autonomous function of SNHG3 [28]. Surprisingly, we found high expression of SNHG3 in exosomes secreted by CAFs isolated from breast cancer patients CAFs which may be important in the progression of breast tumor.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating studies suggested that small nucleolar RNA host genes (SNHGs) could function as endogenous RNAs (ceRNAs) to regulate cancer cells by sponging miRNA, such as miR-182-5p, miR-186-5p and miR-101 [12,27,28]. Therefore, we proposed whether CAF-secreted exosomal SNHG3 could regulate miRNA in cancer cells [18,28]. By bioinformatics analysis and experimental validation, SNHG3 could sponge miR-330 to promote the growth and regulate the metabolism of breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

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SNHG3 Functions as miRNA Sponge to Promote Breast Cancer Cells Growth Through the Metabolic Reprogramming

Zhao

Liu

et al. 2020

Appl Biochem Biotechnol

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Cancer-associated fibroblasts (CAFs) are important ingredient in tumor microenvironment. The dynamic interplay between CAFs and cancer cells plays essential roles during tumor development and progression. However, the mechanisms of intercellular communication between CAFs and cancer cells remain largely unknown. We characterized exosomes secreted from breast cancer patient-derived CAFs by transmission electron microscopy. The expression of SNHG3, miR-330-5p, and PKM (Pyruvate Kinase M1/ M2) was examined by real-time QPCR and immunoblot. The function of SNHG3 on the growth and metabolism of tumor cells was used by CCK8 and mitochondrial oxygen consumption assays. The binding between SNHG3, miR-330-5p, and PKM was examined by dual luciferase reporter assays. Orthotopical xenograft of breast tumor experiments was performed to determine the function of SNHG3 in vivo. We demonstrated that exosomes secreted from CAFs reprogram the metabolic pathways after tumor cells uptake the exosomes. CAF-secreted exosomal lncRNA SNHG3 served as a molecular sponge for miR-330-5p in breast cancer cells. Moreover, PKM could be targeted by miR-330-5p and was controlled by SNHG3 in breast cancer cells. Mechanistically, SNHG3 knockdown in CAF-secreted exosomes suppressed glycolysis metabolism and cell proliferation by the increase of miR-330-5p and decrease of PKM expression in tumor cells. SNHG3 functions as a miR-330-5p sponge to positively regulate PKM expression, inhibit mitochondrial oxidative phosphorylation, increase glycolysis carboxylation, and enhance breast tumor cell proliferation. Overall, SNHG3 could play a major role in the development and progression of breast cancer and support the therapeutic potential of targeting communication between cancer cells and tumor microenvironment.

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Assessment of the expression pattern of mTOR‐associated lncRNAs and their genomic variants in the patients with breast cancer

Taherian‐Esfahani

Taheri

Dashti

et al. 2019

Journal Cellular Physiology

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The mechanistic target of rapamycin (mTOR) is a fundamental component of a signaling pathway that is involved in the pathogenesis of breast cancer via different mechanisms. This pathway is functionally linked with a number of small nucleolar RNA host genes (SNHGs). In the present project, we have searched for the expression quantitative trait loci (eQTLs) within SNHGs that are possibly involved in the pathogenesis of breast cancer. Following this in silico step, we have assessed expression levels of mTOR and four SNHGs in malignant and nonmalignant samples obtained from 80 patients with breast cancer. We also genotyped rs4615861 of SNHG3 and rs3087978 of SNHG5 in the peripheral blood of patients. SNHG12 expression was not detected in any of the assessed malignant or nonmalignant tissues. So this gene was excluded from further steps. Expression of mTOR and other three long noncoding RNAs (lncRNAs) were significantly increased in the malignant tissues compared with the nonmalignant tissues. When classifying patients into down-/upregulation categorized based on the transcript levels of each gene in malignant tissue versus nonmalignant tissues, we noticed associations between expression of SNHG1 and stage (p = 0.03), expression of SNHG5 and grade (p = 0.05), as well as between expression of SNHG3 and history of oral contraceptive use (p = 0.04). We also detected higher levels of SNHG3 expression in estrogen receptor/ progesterone receptor (ER/PR) negative tumors compared with the ER/PR positive tumors (p = 0.003 and p = 0.01, respectively). Moreover, there was a trend toward higher expression of this lncRNA in HER2-positive tumors compared with the HER2negative ones (p = 0.07). Combination of transcript levels of all genes could differentiate malignant tissues from nonmalignant tissues with the diagnostic power of 69% (p = 0.0001). The rs3087978 was associated with the expression of mTOR in malignant tissues in a way that TT and TG genotypes were associated with the higher and lower levels of expressions, respectively (p = 0.01). The current study underscores the significance of SNHGs in the pathogenesis of breast cancer. K E Y W O R D Sbreast cancer, lncRNA, mTOR

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Retracted Article: SNHG3 promotes proliferation and invasion by regulating the miR-101/ZEB1 axis in breast cancer

Abstract: In the present study, we investigated the expression and functional roles of SNHG3 in breast cancer cells, as well as the underlying mechanism of SNHG3 involved in the progression of breast cancer in vitro and in vivo.

Cited by 10 publications

References 39 publications

<p>LncSNHG3/miR-139-5p/BMI1 axis regulates proliferation, migration, and invasion in hepatocellular carcinoma</p>

<p>LncSNHG3/miR-139-5p/BMI1 axis regulates proliferation, migration, and invasion in hepatocellular carcinoma</p>

SNHG3 Functions as miRNA Sponge to Promote Breast Cancer Cells Growth Through the Metabolic Reprogramming

Assessment of the expression pattern of mTOR‐associated lncRNAs and their genomic variants in the patients with breast cancer

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