2019
DOI: 10.1016/j.gene.2019.143960
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LncRNA MIR503HG is downregulated in Han Chinese with colorectal cancer and inhibits cell migration and invasion mediated by TGF-β2

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Cited by 19 publications
(17 citation statements)
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“…Among all the signal pathways that regulate cancer development, the LncRNAs-miRNAs-mRNAs competing endogenous networks are closely associated with the pathogenesis of GC (3)(4)(5)(6), and this study, for the first time, identified a novel LncRNA MIR503HG/miR-224-5p/TUSC3 signaling cascade that regulated unfolded protein response (UPR) to hamper the development of GC. Specifically, we noticed that LncRNA MIR503HG was aberrantly downregulated in GC cells and tissues, and further experiments validated that LncRNA MIR503HG served as a tumor suppressor to reverse the malignant phenotypes and suppress aggressiveness of GC cells in vitro and in vivo, which are supported by the data from other teams in breast cancer (10), bladder cancer (11), and colorectal cancer (9). Then, the principles of ceRNA network mechanisms (12, 13) convince us to investigate the downstream targets of LncRNA MIR503HG, and we successfully screened out that LncRNA MIR503HG sponged miR-224-5p to upregulate TUSC3 in GC cells, and both miR-224-5p overexpression and TUSC3 ablation abrogated the tumor-inhibiting effects of LncRNA MIR503HG on GC, implying that LncRNA MIR503HG regulated the miR-224-5p/ TUSC3 axis to hamper GC progression.…”
Section: Discussionsupporting
confidence: 72%
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“…Among all the signal pathways that regulate cancer development, the LncRNAs-miRNAs-mRNAs competing endogenous networks are closely associated with the pathogenesis of GC (3)(4)(5)(6), and this study, for the first time, identified a novel LncRNA MIR503HG/miR-224-5p/TUSC3 signaling cascade that regulated unfolded protein response (UPR) to hamper the development of GC. Specifically, we noticed that LncRNA MIR503HG was aberrantly downregulated in GC cells and tissues, and further experiments validated that LncRNA MIR503HG served as a tumor suppressor to reverse the malignant phenotypes and suppress aggressiveness of GC cells in vitro and in vivo, which are supported by the data from other teams in breast cancer (10), bladder cancer (11), and colorectal cancer (9). Then, the principles of ceRNA network mechanisms (12, 13) convince us to investigate the downstream targets of LncRNA MIR503HG, and we successfully screened out that LncRNA MIR503HG sponged miR-224-5p to upregulate TUSC3 in GC cells, and both miR-224-5p overexpression and TUSC3 ablation abrogated the tumor-inhibiting effects of LncRNA MIR503HG on GC, implying that LncRNA MIR503HG regulated the miR-224-5p/ TUSC3 axis to hamper GC progression.…”
Section: Discussionsupporting
confidence: 72%
“…Interestingly, their biological functions in regulating GC progression vary according to differential types of LncRNAs, and they act as both tumor suppressors (3,7,8) and oncogenes (4)(5)(6) in GC. Among all the LncRNAs, LncRNA MIR503 host gene (MIR503HG) is located on chromosome Xq26.3, and dysregulated LncRNA MIR503HG contributes to the aggressiveness of multiple cancers (9)(10)(11). Specifically, researcher notice that LncRNA MIR503HG functions as a tumor suppressor to restrain the development breast cancer (10), bladder cancer (11), and colorectal cancer (9), but it is still unclear whether LncRNA MIR503HG involves in regulating GC progression, thus, we selected LncRNA MIR503HG for further investigations in the present study.…”
mentioning
confidence: 99%
“…Chuo et al . [32] demonstrated that MIR503HG overexpression inhibits colorectal cancer cell migration and invasion mediated by transforming growth factor‐β2. Lin et al .…”
Section: Discussionmentioning
confidence: 99%
“…For example, lncRNA LEF1-AS1 was found to accelerate CRC progression by targeting the miR-489/DIAPH1 axis (9). lncRNA MIR503HG alleviated CRC progression by downregulating TGF-β2 expression (10). In addition, lncRNA TTN-AS1 accelerated CRC progression by sponging miR-376a-3p (11).…”
Section: Introductionmentioning
confidence: 99%