Long non-coding RNA SBF2-AS1 promotes hepatocellular carcinoma progression through regulation of miR-140-5p-TGFBR1 pathway

Li, Yu; Liu, Gang; Li, Xiaojun; Dong, Huiyuan; Xiao, Weike; Lu, Shaokang

doi:10.1016/j.bbrc.2018.08.047

Cited by 43 publications

(40 citation statements)

References 27 publications

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“…Of note, activated TGF-β/SMAD signaling serves as a tumor suppressor in early-stage tumors, but acts as a tumor promoter in late-stage tumors (40,41). Consistently, Fukai et al (42) demonstrated that the expression of TGFRβ1 was downregulated in early-stage human esophageal squamous cell carcinoma; however, our results were consistent with those of a recent study by Li et al (43) reporting that TGFβR1 mRNA expression was upregulated in hepatocellular carcinoma, with high mRNA levels of Figure 2. Continued.…”

Section: Discussionsupporting

confidence: 92%

MicroRNA‑133b targets TGFβ receptor I to inhibit TGF‑β‑induced epithelial‑to‑mesenchymal transition and metastasis by suppressing the TGF‑β/SMAD pathway in breast cancer

et al. 2019

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Breast cancer (BC) is one of the most common types of cancer and the leading cause of cancer-associated mortality among women worldwide. Accumulating evidence indicates that microRNA (miR)-133b inhibits the proliferation and invasion of cancer cells. Considering that transforming growth factor (TGF)-β signaling plays a key role in cellular epithelial-to-mesenchymal transition (EMT) and cancer metastasis, it is crucial to explore the roles and underlying molecular mechanisms of miR-133b in regulating TGF-β-induced EMT during progression of BC. In the present study, an inverse correlation was observed between the expression of miR-133b and TGFβ receptor I (TGFβR1) mRNA in BC cells and tissues. Furthermore, miR-133b expression was found to be decreased in the BC tissues of patients with lymph node metastasis and advanced tumor-node-metastasis stage, while the expression of TGFβR1 was upregulated. Overexpression of miR-133b significantly decreased the expression of TGFβR1, an indispensable receptor of TGF-β/SMAD signaling, and suppressed TGF-β-induced EMT and BC cell invasion in vitro, whereas miR-133b knockdown exerted the opposite effects. Mechanistically, TGFβR1 was verified as a direct target of miR-133b as determined by bioinformatics analysis and a dual-luciferase reporter assay. In addition, small interfering RNA-mediated knockdown of TGFβR1 mimicked the phenotype of miR-133b overexpression in BC cells. Furthermore, miR-133b overexpression suppressed BC cell invasion in vivo. Collectively, the findings of the present study indicated that miR-133b acts as a tumor suppressor, inhibiting TGF-β-induced EMT and metastasis by directly targeting TGFβR1, and suppressing the TGF-β/SMAD pathway. Therefore, miR-133b may be of value as a diagnostic biomarker of BC.

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Section: Discussionsupporting

confidence: 92%

MicroRNA‑133b targets TGFβ receptor I to inhibit TGF‑β‑induced epithelial‑to‑mesenchymal transition and metastasis by suppressing the TGF‑β/SMAD pathway in breast cancer

et al. 2019

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“…Gao et al showed that SBF2-AS1 promoted the progression of cervical cancer by regulating miR-361-5p [11]. Li et al found that SBF2-AS1 promotes hepatocellular carcinoma progression through regulation of miR-140-5p-TGFBR1 pathway [19].In the present study, we showd that miR-338-3p was clearly decreased and negatively correlated with SBF2-AS1 expression in GBM. In addition, luciferase reporter and RIP assay showed that SBF2-AS1 acted as a ceRNA to sponge miR-338-3p in GBM progression.…”

Section: Discussionsupporting

confidence: 57%

“…LncRNA SBF2 antisense RNA1 (SBF2-AS1) was initially identi ed in non-small cell lung cancer, which plays the role of oncogene and promotes the occurrence and development of lung cancer, and is closely related to poor prognosis [9]. SBF2-AS1 can adsorb miRNAs (including miR-188-5p, miR-361-5p and miR-140-5p) to promote the evolution and deterioration of acute myeloid leukemia, cervical cancer and liver cancer, respectively [10][11][12]. It was reported that SBF2-AS1was closely related to the occurrence of autophagy in GBM, and which is a tolerance mechanism of cells against tumor therapy [9].…”

Section: Introductionmentioning

confidence: 99%

LncRNA SBF2-AS1 Promotes Malignant Phenotypes and Radioresistance of Glioblastoma Cells by Impairing miR-338-3p-targeted MAP4K3 Inhibition

Pan¹,

Xu²,

Wang³

et al. 2020

Preprint

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Background: Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumors in adults. LncRNA SBF2-AS1 has been reported to promote malignant progression in multiple human cancers. However, the roles and underlying mechanisms of SBF2-AS1 in GBM are still unknown.Methods: The levels of SBF-AS1 were identified in GBM tissues and normal brain tissues, and in GBM cell lines and normal human astrocytes. The effect of SBF2-AS1 on proliferation, invasion and radiosensitivity was evaluated by CCK-8 assay, transwell assay, γ-H2AX foci assay and clonogenic survival assay in vitro and in vivo. The interactions among SBF2-AS1, miR-338-3p and MAP4K3 were validated through luciferase report, RNA immunoprecipitation and western blot assays. Results: In the present study, we comfirmed that SBF2-AS1 was highly upregulated in GBM tissues and cell lines, and its levels were markedly higher in WHO stage III-IV gliomas compared with WHO stage I-II gliomas. Kaplan-Meier survival analysis revealed that glioma patients with high SBF2-AS1 expression had shorter overall survival than those with low SBF2-AS1 expression. SBF2-AS1 inhibition suppressed the proliferation of GBM cells by down-reguating of Ki-67 and CyclinD1. Moreover, silencing SBF2-AS1 increased the proportion of cells in G1 phase and decreased the proportion of cells in S phase. In addition, SBF2-AS1 inhibition suppressed the invasion of GBM cells by down-reguating of MMP2 and MMP9. Xenograft tumor models revealed that the silencing of SBF2-AS1 inhibited tumor growth in vivo. Moreover, the silencing of SBF2-AS1 significantly sensitized GBM cells to radiation in vitro and in vivo. Indeed, we observed a persistence of γ-H2AX staining after ionizing radiation, leading to enhanced DNA repair and radioresistance. Mechanistically, SBF2-AS1 inhibition reduced the expression of MAP4K3 by directly binding with miR-338-3p in GBM cells. Conclusions: Our study demonstrated that SBF2-AS1 enhanced cell proliferation, invaison and radioresistance via modulating miR-338-3p/MAP4K3 axis, and it is an attractive therapeutic target to overcome radioresistance of GBM.

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“…The cell culture method has been reported before. 15 Lentivirus was produced by GeneChemCo., Ltd. (Shanghai, People's Republic of China). For lentivirus infection, HCC cells were plated in 6-well plates and 100 μL lentivirus (virus titer, 10 9 TU/ml) was added.…”

Section: Cell Lines and Transfectionmentioning

confidence: 99%

<p>LINC00339 promotes growth and invasiveness of hepatocellular carcinoma by the miR-1182/SKA1 pathway</p>

Xiao¹,

Yu²,

Ma³

2019

OTT

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Background: Extensive research has shown that long noncoding RNA (lncRNA) is involved in tumorigenesis, including hepatocellular carcinoma (HCC). The lncRNA LINC00339 was reported to regulate the development of lung cancer or breast cancer. However, whether LINC00339 participates in HCC progression remains unclear. Here, our results showed that LINC00339 was upregulated in HCC. Methods: qRT-PCR and in situ hybridization (ISH) was used to analyze LINC00339 expression in tumor tissues and cell lines. CCK8 and colony formation assays were used to analyze cell proliferation. Transwell assay was used to analyze cell migration and invasion. Xenograft experiment was used to test tumor growth in vivo. Results: LINC00339 overexpression was correlated with an advanced stage, metastasis, and bad prognosis in HCC patients. Functional investigation showed that LINC00339 knockdown significantly suppressed HCC cell proliferation, migration, and invasion. Moreover, decreased LINC00339 expression inhibited HCC growth in vivo. Mechanistically, LINC00339 could interact with miR-1182 to promote SKA1 expression. We also demonstrated that SKA1 acted as an oncogene and SKA1 upregulation reversed the effect of LINC00339 silencing. Conclusion: Our results illustrated that the LINC00339/miR-1182/SKA1 axis plays an essential role in HCC progression.

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Long non-coding RNA SBF2-AS1 promotes hepatocellular carcinoma progression through regulation of miR-140-5p-TGFBR1 pathway

Cited by 43 publications

References 27 publications

MicroRNA‑133b targets TGFβ receptor I to inhibit TGF‑β‑induced epithelial‑to‑mesenchymal transition and metastasis by suppressing the TGF‑β/SMAD pathway in breast cancer

MicroRNA‑133b targets TGFβ receptor I to inhibit TGF‑β‑induced epithelial‑to‑mesenchymal transition and metastasis by suppressing the TGF‑β/SMAD pathway in breast cancer

LncRNA SBF2-AS1 Promotes Malignant Phenotypes and Radioresistance of Glioblastoma Cells by Impairing miR-338-3p-targeted MAP4K3 Inhibition

<p>LINC00339 promotes growth and invasiveness of hepatocellular carcinoma by the miR-1182/SKA1 pathway</p>

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