RETRACTED ARTICLE: MiRNA-211 suppresses cell proliferation, migration and invasion by targeting SPARC in human hepatocellular carcinoma

Deng, Bingbing; Qu, Lei; Li, Jinfang; Fang, Jie; Yang, Shouwen; Cao, Zhongwei; Mei, Zhechuan; Sun, Xiaojiang

doi:10.1038/srep26679

Cited by 42 publications

(32 citation statements)

References 30 publications

(40 reference statements)

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“…The secreted protein acidic and rich in cysteine (SPARC; alternative names: osteonectin; ON or basement membrane-40; BM-40) family is recognized as extracellular matrix proteins[6]. A differential expression of SPARC in tumor tissue and its surrounding stroma compared to normal tissues has been reported for many different types of cancer[7].…”

Section: Introductionmentioning

confidence: 99%

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Su¹,

Kuai²,

Li³

2016

WJG

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AIMTo determine the influence of Smoc2 on hepatocellular carcinoma (HCC) cell proliferation and to find a possible new therapeutic target for preventing HCC progression.METHODSWe detected expression of Smoc2 in HCC tissues and corresponding non-tumor liver (CNL) tissues using PCR, western blot, and immunohistochemistry methods. Subsequently, we down-regulated and up-regulated Smoc2 expression using siRNA and lentivirus transfection assay, respectively. Then, we identified the effect of Smoc2 on cell proliferation and cell cycle using CCK-8 and flow cytometry, respectively. The common cell growth signaling influenced by Smoc2 was detected by western blot assay.RESULTSThe expression of Smoc2 was significantly higher in HCC tissues compared with CNL tissues. Overexpression of Smoc2 promoted HCC cell proliferation and cell cycle progression. Down-regulation of Smoc2 led to inhibition of cell proliferation and cell cycle progression. Smoc2 had positive effect on ERK and AKT signaling.CONCLUSIONSmoc2 promotes the proliferation of HCC cells through accelerating cell cycle progression and might act as an anti-cancer therapeutic target in the future.

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Section: Introductionmentioning

confidence: 99%

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Su¹,

Kuai²,

Li³

2016

WJG

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“…On the one hand, SPARC acts as a tumor suppressor to inhibit migration and invasion of breast cancer cells and inhibits tumor growth and angiogenesis in neuroblastoma . However, SPARC has also been reported to act as a tumor promotor that is closely related to cell adhesion, migration, metastasis, poor prognosis, and remodeling . In our study, we examined subcutaneous tumor formation in nude mice.…”

Section: Discussionmentioning

confidence: 99%

“…10,33 However, SPARC has also been reported to act as a tumor promotor that is closely related to cell adhesion, migration, metastasis, poor prognosis, and remodeling. [34][35][36] In our study, we examined subcutaneous tumor formation in nude mice. We found that tumor size in SPARCoverexpressing tumors was larger than in the control group.…”

Section: Discussionmentioning

confidence: 99%

Secreted protein acidic and rich in cysteine promotes epithelial–mesenchymal transition of hepatocellular carcinoma cells and acquisition of cancerstem cell phenotypes

Jiang

Liu

Wang

2019

J of Gastro and Hepatol

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Background and Aim Secreted protein acidic and rich in cysteine (SPARC) is a matricellular glycoprotein that plays a significant role in tumor development. SPARC has been indicated that promotes tumorigenesis, metastasis, and poor prognosis in prostate cancer and lung cancer. Therefore, we sought to investigate the molecular mechanisms of SPARC in regulating hepatocellular carcinoma (HCC). Methods We used spheroids cultured in serum‐free culture medium to obtain liver cancer stem cells. Flow cytometric analysis was performed to investigate percentage of CD133+ cells in liver cancer cells. Real‐time polymerase chain reaction and western blot were used to assess gene expression in cell lines. Transwell and wound healing assays were performed to indicate cell migration of HCC. Results Secreted protein acidic and rich in cysteine was upregulated in spheres formation in HCC cells. Overexpression of SPARC enhanced the ability to form tumor spheres and increased CD133 and Oct4 expressions. Besides, SPARC promoted the migration and epithelial–mesenchymal transition in HCC cells. Importantly, SPARC overexpression stimulated the formation of subcutaneous tumors in nude mice. Conclusions Our findings suggest that SPARC overexpression promotes tumor growth, inducing epithelial–mesenchymal transition and acquisition of a stem cell phenotype. What is more, research elucidating the biological mechanisms of SPARC may be beneficial to liver cancer treatment.

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“…SPARC was reported to be involved in prostate cancer migration into bone and promoted glioma cell motility and invasion . SPARC contributed to the migration and invasion of human hepatocellular carcinoma . By decreasing type IV collagen levels, SPARC promoted cell invasion in vivo .…”

Section: Discussionmentioning

confidence: 99%

SPARC acts as a mediator of TGF‐β1 in promoting epithelial‐to‐mesenchymal transition in A549 and H1299 lung cancer cells

et al. 2018

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Migration and metastasis of tumor cells greatly contributes to the failure of cancer treatment. Recently, the extracellular protein secreted protein acidic and rich in cysteine (SPARC) has been reported closely related to tumorigenesis. Some articles have suggested that SPARC promoted metastasis in several highly metastatic tumors. However, there are also some studies shown that SPARC acted as an antitumor factor. SPARC-induced epithelial-tomesenchymal transition (EMT) in melanoma cells and promoted EMT in hepatocellular carcinoma. Therefore, the role of SPARC in tumorigenesis and its relationship with EMT is still unclear. In this study, we investigated the expression change of SPARC in A549 and H1299 lung cancer cells undergoing EMT process. Our study indicated that SPARC was upregulated in A549 and H1299 cells EMT process. We further investigated the function of SPARC on proliferation, migration, and EMT process of A549 and H1299 cells. Overexpression of SPARC promoted the migration and EMT of A549 and H1299 cells. Knockdown SPARC inhibited the EMT of A549 cells. Overexpression of SPARC induced the increased expression of p-Akt and P-ERK. Furthermore, exogenous SPARC peptide promoted transforming growth factor (TGF)-β1-induced EMT of A549 and H1299 cells. SPARC knockdown partially eliminated TGF-β1 function in inducing EMT of A549 cells. SPARC follistatin-like functional domain reduced the expression of E-cadherin, but had no effect on the expression of p-Akt and p-ERK. In conclusion, we elucidated that SPARC contributes to tumorigenesis by promoting migration and EMT of A549 and H1299 lung cancer cells. These results will provide some new suggestion for lung cancer treatment. © 2018 BioFactors, 44(5):453-464, 2018Abbreviations: A549, A human lung adenocarinoma epithelial cell line; Akt, A serine/threonine-specific protein kinase; BSA, bovine serum albumin; CCK-8, cell counting kit-8; DMEM, Dulbecco's modified Eagle's Medium; EC, extracellular calcium-binding domain; EDTA, ethylenediaminetetraacetic acid; EGFP, enhancer green fluorescent protein; EGF, epidermal growth factor; EMT, epithelial-to-mesenchymal transition; ERK, extracellular signal-regulated kinases; FBS, fetal bovine serum; FS, follistatin-like functional domain; Fyn, Fyn proto-oncogene, Src family tyrosine kinase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; H1299, A human non-small cell lung carcinoma cell line; ILK, integrin-linked kinase; MDM2, mouse double minute 2 homolog; NF-κB, nuclear factor kappa B subunit 1; Nab-PTX, nanoparticle albumin bound paclitaxel; NSCLC, nonsmall cell lung cancer; NT, N terminal acidic domain; PBS, phosphate-buffered saline; PARP, poly (ADP-ribose) polymerase 1; PMSF, phenylmethane sulfonyl fluoride; RIPA, radioimmunoprecipitation assay buffer; SDS, sodium dodecyl sulfate; SPARC, secreted protein acidic and rich in cysteine; TGF-β, transforming growth factor; TBST, a mixture of tris-buffered saline and Tween 20 Additional Supporting Information may be found in the online version of this article.

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RETRACTED ARTICLE: MiRNA-211 suppresses cell proliferation, migration and invasion by targeting SPARC in human hepatocellular carcinoma

Cited by 42 publications

References 30 publications

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Secreted protein acidic and rich in cysteine promotes epithelial–mesenchymal transition of hepatocellular carcinoma cells and acquisition of cancerstem cell phenotypes

SPARC acts as a mediator of TGF‐β1 in promoting epithelial‐to‐mesenchymal transition in A549 and H1299 lung cancer cells

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