LINC01410 promotes cell proliferation and migration of cholangiocarcinoma through modulating miR‐124‐3p/SMAD5 axis

Abstract

Background: Cholangiocarcinoma (CCA) is generally associated with high incidence and poor prognosis. Nowadays, increasing experimental data demonstrate that long non-coding RNA (lncRNA) plays an indispensable role in tumor occurrence.Nevertheless, the specific mechanism of lncRNA is not clear in CCA. Methods:The relative expressions of lncRNAs, miRNAs, and mRNAs were detected by real-time quantitative PCR (RT-qPCR). CCK8 and colony formation assays were applied to examine cell proliferation ability in CCA. Transwell assay was conducted to measure the migration and invasion capabilities of CCA cells.Nuclear and cytoplasmic separation assay was implemented to figure out the location of LINC01410. Luciferase reporter assay, RIP and RNA pull-down assays were applied to certify the molecular bindings. Western blot was applied to detect the protein level.Results: The high expression of LINC01410 was proved in CCA tissues and CCA cell lines. Also, CCA patients with high LINC01410 level presented poor prognosis. LINC01410 deficiency impeded cell proliferation, migration and invasion in HuCCT1and RBE cell lines. What's more, LINC01410 interacted with miR-124-3p. Meanwhile, SMAD5 targeted and inhibited by miR-124-3p. SMAD5 expression was enhanced by LINC01410.Conclusion: LINC01410 facilitates cell proliferation, migration and invasion through miR-124-3p/SMAD5 axis.

Long noncoding RNA LINC01410 promotes the tumorigenesis of neuroblastoma cells by sponging microRNA‐506‐3p and modulating WEE1

“…Knockdown of LINC01410 attenuates cell growth and arrests cell cycle at G0/G1 phase via suppressing miR‐3128 in colon cancer 11 . LINC01410 serves as an oncogenic that accelerates cholangiocarcinoma tumorigenesis by modulating the expression of SMAD5 via directly targeting miR‐124‐3p 12 . In this study, LINC01410 knockdown restrained cell proliferation and colony formation ability, and arrested cell cycle, and accelerates cell apoptosis, suggesting that LINC01410 plays pivotal roles in the modulation of NBL progression in vitro.…”

“…Here, the LINC01410 expression was markedly enhanced in NBL tissues and cells. Notably, LINC01410 is high‐expressed in diverse tumors, including gastric cancer, 13 cervical cancer, 33 and cholangiocarcinoma 12 . In this study, high LINC01410 expression was positively associated with WHO grade in NBL patients, and conferred a survival disadvantage to NBL patients.…”

“…For instance, LINC01410 accelerates tumorigenesis of colon cancer through suppressing miR‐3128 11 . LINC01410 regulates miR‐124‐3p to increase the SMAD5 expression, elevating cholangiocarcinoma cell proliferation, and migration rates 12 . LINC01410 contributes to angiogenesis and metastasis in gastric cancer via inhibiting the miR‐532‐5p expression 13 .…”

Emerging roles of long noncoding RNAs in cholangiocarcinoma: Advances and challenges

“…Studies from different groups have confirmed that the dysregulation of lncRNA expression is closely related to the biological behavior of CCA cells. Upregulation of these lncRNAs, including KCNQ1OT1 [48], LMCD1-AS1 [37], TP73-AS1 [22], SNHG1 [49], SOX2-OT [39], LINC01410 [50], ASAP1-IT1 [51], DANCR [52], FLVCR1-AS1 [53], NNT-AS1 [54], RMRP [55], CCAT2 [56], HOTAIR [57], LINC01296 [58], LOXL1-AS1 [59], NEAT1 [60], PVT1 [43], HEIH [61], LINC01061 [62], may promote the migration and invasion of CCA cells, . On the other hand, the downregulation of several lncRNAs plays the same role in CCA cells including LINC01714 [63], FENDRR [64], MEG3 [65], and MIR22HG [66].…”

Identification of novel prognostic markers of survival time in high-risk neuroblastoma using gene expression profiles

“…LINC01410 is a lncRNA highly expressed in pancreatic cancer tissues and cell lines [52]. High expression in cholangiocarcinoma and gastric cancer patients have been associated with poor prognosis and survival [53,54]. These lncRNAs may be facilitating the promotion of tumor progression, proliferation and invasion which might have impacted the survival of patients in the short survival group.…”