MiR-422a weakened breast cancer stem cells properties by targeting <i>PLP2</i>

Zou, Yanmei; Chen, Yuandong; Yao, Shuo; Deng, Guo-Min; Liu, Dian; Liu, Shunfang; Rao, J. V.; Xiong, Huihua; Yuan, Xianglin; Yu, Shiying; Feng, Zheng; Wang, Yihua; Xiong, Hua

doi:10.1080/15384047.2018.1433497

Cited by 36 publications

(39 citation statements)

References 18 publications

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“…Interestingly, miR-449a has been reported to suppress cell migration and invasion in NSCLC by targeting c-Met [8]. Likewise, miR-422a up-regulation has been found to restrain microsphere formation, cell growth and tumorigenesis by inhibiting PLP2 expression in breast cancer [25]. Evidence has been presented supporting SULF2 as a target of miR-422a and can be negatively regulated by miR-422a by dual luciferase reporter gene assay and western blot assay.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-422a functions as a tumor suppressor in non-small cell lung cancer through SULF2-mediated TGF-β/SMAD signaling pathway

Zhang

Wang

et al. 2019

Cell Cycle

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MicroRNAs (miRNAs) have been demonstrated to participate in a variety of human cancers by functioning as post-transcriptional regulators of oncogenes or antioncogenes including non-small cell lung cancer (NSCLC). The aim of the current study was to identify the role of miR-422a in NSCLC via sulfatase 2 (SULF2) to further elucidate the mechanism of NSCLC. Initially, the expression of miR-422a and SULF2 was determined in NSCLC tissues and cells. The role of miR-422a in NSCLC was identified in relation with a miR-422a mimic or inhibitor, siRNA against SULF2 and TGF-β1. The regulatory effects of miR-422a were examined following detection of the related epithelial mesenchymal transition (EMT)-related genes, and the apoptosis-related genes and evaluation of their cellular biological functions. The expression pattern of miR-422a, SULF2, and the TGF-β/ SMAD pathway-related genes was detected to elucidate the mechanism by which miR-422a influences the progression of NSCLC. Finally, xenograft tumors in nude mice were observed for tumorigenicity evaluation purposes. Our results showed that miR-422a was poorly expressed while SULF2 was highly expressed in NSCLC. Dual luciferase reporter gene assay further verified that miR-422a targeted SULF2. Altogether, this study demonstrated that miR-422a downregulated SULF2 to inhibit the TGF-β/SMAD pathway. NSCLC cell proliferation, migration, invasion, colony formation, EMT and tumorigenesis were all inhibited while apoptosis was promoted upon restoration of miR-422a or silencing of SULF2. However, the activation of the TGF-β/SMAD pathway was determined to reverse the tumor-suppressive effects of si-SULF2. miR-422a restoration, which ultimately inhibited the progression of NSCLC by suppressing the TGF-β/SMAD pathway via SULF2.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-422a functions as a tumor suppressor in non-small cell lung cancer through SULF2-mediated TGF-β/SMAD signaling pathway

Zhang

Wang

et al. 2019

Cell Cycle

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“…Previous studies have uncovered that miR-422a functions as a tumor suppressor in a variety of F I G U R E 3 Upregulation of miR-422a inhibits RB proliferation in vitro. 19 Here in this study we found that miR-422a negatively modulated SKP2 and suppressed proliferation of RB cells. B, Clonogenic capacity of cells treated with miR-422a mimics or NC-mimics was measured by colony formation assay.…”

Section: Discussionsupporting

confidence: 48%

SKP2, positively regulated by circ_ODC1/miR‐422a axis, promotes the proliferation of retinoblastoma

Wang

Zhang

et al. 2019

J of Cellular Biochemistry

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Retinoblastoma (RB) is the most common intraocular malignancy in infants and children. S‐phase kinase‐associated protein 2 (SKP2) has been unmasked as an oncogene in a great many of carcinomas. The biologic function and the detailed molecular mechanism of SKP2 in RB need to be better understood. In this study, real‐time quantitative polymerase chain reaction and Western blot showed the ectopic expression of SKP2 in RB tissues and cell lines. Loss of function assays showed the attenuated cell proliferation in RB as a result of SKP2 knockdown. In addition, bioinformatics analysis predicted the interaction between SKP2 and miR‐422a. Luciferase reporter assay and Pearson's correlation analysis validated the negative correlation between miR‐422a and SKP2. MiR‐422a overexpression led to a decline of SKP2 expression and cell growth in RB. The binding capacity between miR‐422a and circ_ODC1 was also predicted by bioinformatics analysis. Pearson's correlation analysis and luciferase reporter assay confirmed that circ_ODC1 is negatively correlated with miR‐422a. Silencing circ_ODC1 resulted in a rise in miR‐422a expression and RB cell growth. Moreover, reduced cell growth was restored by SKP2 overexpression. In a word, SKP2, induced by circ_ODC1 and miR‐422a, promotes RB proliferation. Our new findings in this research might expedite the discovery of novel prognostic markers and therapeutic targets of RB.

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“…Clinical data analysis found that miR-765 had a negative association with PLP2 in human ccRCC samples. PLP2 was shown to function as an oncogene in hepatocellular carcinoma [30], breast cancer [31] and glioma [32]. However, the function of PLP2 and miRNAs in regulating PLP2 expression in ccRCC remains unknown.…”

Section: Discussionmentioning

confidence: 99%

MiR-765 functions as a tumour suppressor and eliminates lipids in clear cell renal cell carcinoma by downregulating PLP2

et al. 2020

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A B S T R A C TBackground: Lipid accumulation has been highlighted in cancer development and progression, but the exact mechanism remains unclear in renal cell carcinoma (RCC). MicroRNAs (miRNAs) have been confirmed to participate in the pathological processes of cancers, including tumour occurrence and inhibition. However, the role and mechanism of miR-765 have not been elucidated in clear cell renal cell carcinoma (ccRCC). Methods: Using The Cancer Genome Atlas (TCGA) database and qRT-PCR, we investigated differences in miR-765 and proteolipid protein 2 (PLP2) expression, as well as their clinical relevance. To investigate the function of miR-765 and PLP2 in ccRCC, we performed in vitro and in vivo experiments to explore their biological functions in ccRCC. Findings: In this study, we showed that miR-765 was upregulated in the plasma of ccRCC patients after tumour resection. Consistently, ccRCC tissues had low expression of miR-765 when compared with corresponding non-cancerous tissues. Overexpression of miR-765 suppressed cell proliferation and metastasis in vitro and in vivo. Mechanistic studies demonstrated that PLP2 was a direct target gene of miR-765. PLP2 was highly expressed in ccRCC tissues, and high PLP2 levels were positively correlated with higher tumour stage and grade and poor prognosis. PLP2 expression was negatively correlated with the miR-765 level in patient samples. We further showed that PLP2 restrained the cell metastasis and proliferation induced by miR-765 and reduced the lipid-eliminating effects of miR-765 in renal cancer cells. Interpretation: Our findings suggest that miR-765 may function as a tumour suppressor and eliminate lipids in clear cell renal cell carcinoma by targeting PLP2. EBioMedicine journal homepage: www.elsevier.com/locate/ebiom that miR-765 inhibits osteosarcoma [23] and tongue squamous cell carcinoma [24]. Nevertheless, to the best of our knowledge, there is still no relevant research about the role of miR-765 in ccRCC. We found that the plasma level of miR-765 was upregulated after tumour resection in ccRCC patients and that ccRCC tissues had a low level of miR-765 compared with corresponding non-ccerous tissues. The present study systematically describes the function and role of miR-765 in ccRCC. Functionally, miR-765 inhibited RCC cell proliferation, migration and invasion in vitro and in vivo. Mechanistically, miR-765 serves as a tumour suppressor and eliminates lipids by downregulating PLP2 in ccRCC. Our findings reveal that the miR-765-PLP2 axis may be a biomarker and a therapeutic target for ccRCC. Materials and methods Patient samples and cellsThirty-six clear cell renal cell carcinoma (ccRCC) patient surgical specimens, 18 non-ccRCC (nccRCC) patient surgical specimens and 18 blood plasma samples (preoperative and operational day 7 without chemotherapy or radiotherapy for ccRCC) were obtained from

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MiR-422a weakened breast cancer stem cells properties by targeting PLP2

Abstract: Up-regulation of miR-422a attenuated microsphere formation, proliferation and tumor formation of breast cancer stem cells via suppressing the PLP2 expression.

Cited by 36 publications

References 18 publications

RETRACTED ARTICLE: MicroRNA-422a functions as a tumor suppressor in non-small cell lung cancer through SULF2-mediated TGF-β/SMAD signaling pathway

RETRACTED ARTICLE: MicroRNA-422a functions as a tumor suppressor in non-small cell lung cancer through SULF2-mediated TGF-β/SMAD signaling pathway

SKP2, positively regulated by circ_ODC1/miR‐422a axis, promotes the proliferation of retinoblastoma

MiR-765 functions as a tumour suppressor and eliminates lipids in clear cell renal cell carcinoma by downregulating PLP2

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