Knockdown of LINC00467 contributed to Axitinib sensitivity in hepatocellular carcinoma through miR-509-3p/PDGFRA axis

Li, Wei; He, Yingna; Chen, Wei; Man, Wenling; Fu, Qiang; Tan, Hongtong; Guo, Huanqing; Zhou, Jingnan; Yang, Po Song

doi:10.1038/s41434-020-0137-9

Cited by 22 publications

(23 citation statements)

References 38 publications

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“…The first study about LINC00467 revealed its carcinogenic functions in neuroblastoma; LINC00467 silencing decreased the proliferation of tumor cells but enhanced apoptosis, indicating that LINC00467 functions as a tumor repressor ( 15 ). A previous study revealed that LINC00467 promoted proliferation and invasion, inhibited apoptosis, and contributed to axitinib resistance in hepatocellular carcinoma through miR-509-3p/PDGFRA ( 18 ). Another study demonstrated that LINC00467 enhances the progression of non-small cell lung cancer through the AKT signaling cascade, and TDG-induced acetylation is the pivotal factor that modulates the expression of LINC00467 ( 16 ).…”

Section: Discussionmentioning

confidence: 99%

LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis

et al. 2021

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BackgroundThe long non-coding RNA LINC00467 plays a vital role in many malignancies. Nevertheless, the role of LINC00467 in prostate carcinoma (PC) is unknown. Herein, we aimed to explore the mechanism by which LINC00467 regulates PC progression.MethodsWe used bioinformatics analyses and RT-qPCR to investigate the expression of LINC00467 in PC tissues and cells. The function of LINC00467 in the progression of PC was confirmed by loss-of-function experiments. PC cell proliferation was assessed by CCK-8 and EdU assays. The cell cycle progression of PC cells was examined by flow cytometry. Moreover, Transwell assays were used to investigate the migration and invasion of PC cells. Western blot assays were used to detect the expression of factors associated with epithelial–mesenchymal transition. The interactions of LINC00467 with prostate cancer progression and M2 macrophage polarization were confirmed by RT-qPCR. The subcellular localization of LINC00467 was investigated via the fractionation of nuclear and cytoplasmic RNA. Bioinformatics data analysis was used to predict the correlation of LINC00467 expression with miR-494-3p expression. LINC00467/miR-494-3p/STAT3 interactions were identified by using a dual-luciferase reporter system. Finally, the influence of LINC00467 expression on PC progression was investigated with an in vivo nude mouse model of tumorigenesis.ResultsWe established that LINC00467 expression was upregulated in PC tissues and cells. Downregulated LINC00467 expression inhibited PC cell growth, cell cycle progression, migration, and invasion. Downregulated LINC00467 expression similarly inhibited PC cell migration via M2 macrophage polarization. Western blot analysis showed that LINC00467 could regulate the STAT3 pathway. We established that LINC00467 is mainly localized to the cytoplasm. Bioinformatics analysis and rescue experiments indicated that LINC00467 promotes PC progression via the miR-494-3p/STAT3 axis. Downregulated LINC00467 expression was also able to suppress PC tumor growth in vivo.ConclusionsOur study reveals that LINC00467 promotes prostate cancer progression via M2 macrophage polarization and the miR-494-3p/STAT3 axis.

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Section: Discussionmentioning

confidence: 99%

LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis

et al. 2021

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“…These studies also demonstrated that linc00467 upregulated in HCC tissues and cells, performing diverse functions in tumorigenesis, metastasis, and cancer progression [ 23–26 ]. Previous studies have reported that linc00467 promotes cell proliferation and metastasis through insulin-like growth factor-2 messenger RNA-binding protein 3/tumor necrosis factor receptor-associated factor 5, miR-18a-5p/neural precursor cell expressed developmentally down-regulated 9, miR-509-3p/platelet-derived growth factor receptor alpha pathways, indicating linc00467 signaling may impede apoptosis, and contribution to axitinib resistance of HCC, these results indicated that linc00467 may serve as a promising biomarker and target for HCC treatment [ 23 , 25 , 26 ]. However, different from linc00467 upregulation in cancer cells, a study by Kerui Cai et al reported that linc00467 was aberrantly decreased in HCC, especially in metastases [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

Linc00467 promotion of gastric cancer development by directly regulating miR-7-5p expression and downstream epidermal growth factor receptor

et al. 2021

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Linc00467 is a vital regulator in tumor progression. This study explores the molecular mechanisms of linc00467 in gastric cancer (GC). Linc00467 expression was obtained and analyzed in GC tissue through exploration in the cancer genome atlas database. Then, real-time quantitative polymerase chain reaction was used to detect linc000467 expression in GC cells. Cell functions were observed using cell counting Kit-8, Transwell assay, Western blotting to testify the proliferation, migration, invasion, and the relative expression of epidermal growth factor receptor (EGFR) in GC cells. Moreover, a dual-luciferase reporter gene assay was used to verify the relationship between linc00467 and miR-7-5p. Results showed that the expression of linc00467 was overexpressed in GC. Linc00467 silencing decreased the GC cell proliferation, migration, and invasion. With mRNA verification and combined previous research, linc00467 directly regulated the miR-7-5p expression and downstream EGFR expression. Inhibited miR-7-5p could restore cell function, EGFR expression of GC cells when linc00467 knockdown occurs. Altogether, linc00467 directly regulates the miR-7-5p and EGFR signaling pathway to promote GC proliferation, migration, and invasion.

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“…A previous review has shown that lncRNAs serve important roles in numerous biological processes, including differentiation, proliferation and metabolism, and also have crucial functions in disease pathogeneses, particu-larly cancer ( 12 ). Differentially expressed lncRNAs have been observed in HCC by several studies ( 13 – 15 ), suggesting a crucial role of lncRNAs in HCC. Moreover, lncRNAs exhibit cancer-inhibiting or cancer-promoting activities and are implicated in the regulation of pathological processes in malignant cells ( 16 ).…”

Section: Introductionmentioning

confidence: 96%

Long non‑coding RNA MKLN1‑AS aggravates hepatocellular carcinoma progression by functioning as a molecular sponge for miR‑654‑3p, thereby promoting hepatoma‑derived growth factor expression

Gao¹,

Chen²,

Chi³

et al. 2020

Int J Mol Med

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Long non-coding RNAs (lncRNAs) have recently gained attention due to their important roles in human cancer types, such as breast and gastric cancer. The present study measured alterations in muskelin 1 antisense RNA (MKLN1-AS) expression in hepatocellular carcinoma (Hcc) and evaluated its clinical value in patients with Hcc. Additionally, the current study investigated the effects of MKLN1-AS on the malignant features of Hcc cells. The detailed molecular mechanisms underlying the cancer-promoting activities of MKLN1-AS in Hcc cells were also elucidated. MKLN1-AS expression in Hcc tissues and cell lines was detected using reverse-transcription quantitative PCR (RT-qPCR). Cell Counting Kit-8 assays and flow cytometry were used to determine the roles of MKLN1-AS in Hcc cell proliferation and apoptosis. Migration and invasion assays, as well as tumor xenograft experiments were conducted to analyze migration and invasion in vitro and tumor growth in vivo, respectively. The interaction among microRNA-654-3p (miR-654-3p), MKLN1-AS and hepatoma-derived growth factor (HdGF) in Hcc was investigated using luciferase reporter assay, RNA immunoprecipitation assay, RT-qPcR, western blotting and rescue experiments. MKLN1-AS was upregulated in Hcc tissues and cell lines, and a high MKLN1-AS expression was associated with shorter overall survival and disease-free survival in patients with Hcc. Functionally, the knockdown of MKLN1-AS impaired Hcc cell proliferation, migration and invasion, as well as induced cell apoptosis in vitro. Knockdown of MKLN1-AS expression also inhibited cell proliferation in vivo. The results indicated that MKLN1-AS functioned as a competing endogenous RNA by sponging miR-654-3p in Hcc cells. Additionally, miR-654-3p targeting of HdGF was positively modulated by MKLN1-AS, and miR-654-3p knockdown partially abrogated this effect. Rescue experiments demonstrated that knockdown of miR-654-3p and overexpression of HdGF both abolished MKLN1-AS knockdown-induced cellular processes in Hcc. In summary, MKLN1-AS induced pro-oncogenic effects during Hcc progression by serving as a molecular sponge for miR-654-3p to increase HdGF expression. Therefore, the MKLN1-AS/miR-654-3p/HdGF axis may offer a novel target for the diagnosis, prognosis, prevention and treatment of Hcc.

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Knockdown of LINC00467 contributed to Axitinib sensitivity in hepatocellular carcinoma through miR-509-3p/PDGFRA axis

Cited by 22 publications

References 38 publications

LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis

LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis

Linc00467 promotion of gastric cancer development by directly regulating miR-7-5p expression and downstream epidermal growth factor receptor

Long non‑coding RNA MKLN1‑AS aggravates hepatocellular carcinoma progression by functioning as a molecular sponge for miR‑654‑3p, thereby promoting hepatoma‑derived growth factor expression

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