LINC00707 contributes to hepatocellular carcinoma progression via sponging miR‐206 to increase CDK14

  title={LINC00707 contributes to hepatocellular carcinoma progression via sponging miR‐206 to increase CDK14},
  author={Jian-fei Tu and Zhongwei Zhao and Min Xu and Minjiang Chen and Qiaoyou Weng and Jiangmei Wang and Jiansong Ji},
  journal={Journal of Cellular Physiology},
  pages={10615 - 10624}
Recently, increasing numbers of long noncoding RNAs (lncRNAs) have been found to be aberrantly expressed in various cancers. However, the roles of lncRNAs in hepatocellular carcinoma (HCC) progression is largely unknown. In our current study, we identified that long intergenic nonprotein‐coding RNA 707 (LINC00707) was remarkably elevated in HCC cells, indicating that LINC00707 was involved in HCC development. Subsequently, LINC00707 was significantly decreased in HepG2 and Huh7 cells. The in… 

LINC00707 accelerates the proliferation, migration and invasion of clear cell renal cell carcinoma.

LINC00707 is upregulated in ccRCC, which could promote cancer cells to proliferate, migrate, and invade, and accelerates the progression ofccRCC by activating EMT pathway.

LncRNA LOC105372579 promotes proliferation and epithelial-mesenchymal transition in hepatocellular carcinoma via activating miR-4316/FOXP4 signaling

Findings supported that LOC105372579 contributes to HCC cell proliferation, migration, invasion, and EMT by activating miR-4316/FOXP4 signaling.

Hypoxia associated lncRNA HYPAL promotes proliferation of gastric cancer as ceRNA by sponging miR-431-5p to upregulate CDK14

HIF-1α/HYPAL/miR-431-5p/CDK14/Cyclin-dependent kinase 14 axis activated the Wnt/β-catenin signaling pathway and induced GC cell proliferation while inhibiting apoptosis and is a potential molecular target for GC therapy.

UNC5B-AS1 promotes the proliferation, migration and EMT of hepatocellular carcinoma cells via regulating miR-4306/KDM2A axis

Results showed UNC5B-AS1 was upregulated in HCC tissues and cells, contributing to the development of cancer staging and survival rate of HCC patients and accelerates the proliferation, migration and EMT of H CC cells via the regulation of miR-4306/KDM2A axis.

LINC00707 Promotes Cell Proliferation in Cervical Cancer via the miR-374c-5p/SDC4 Axis

Data of rescue assays proved that LINC00707 could promote CC cell malignancy via the miR-374c-5p/SDC4 axis, which revealed a potential treatment option for CC.

Long non-coding RNA LINC00707 acts as a competing endogenous RNA to enhance cell proliferation in colorectal cancer.

The upregulation of LINC00707 expression was significantly associated with tumor size, stage and poor survival in patients with CRC and is associated with a shorter survival time in patientswith CRC.

Long noncoding RNA SNHG7 represses the expression of RBM5 to strengthen metastasis of hepatocellular carcinoma.

This study suggests that SNHG7 could promote cell invasion and migration in HCC cells through downregulating RBM5, which may offer a new therapeutic intervention for HCC patients.

The Impact of Long Non-Coding RNAs in the Pathogenesis of Hepatocellular Carcinoma

The recent finding about the impact of lncRNAs in HCC is described, which indicates that a number of so-called tumor suppressor lnc RNAs namely CASS2 and MEG3 are down-regulated in H CC.

miR-206-G6PD axis regulates lipogenesis and cell growth in hepatocellular carcinoma cell

It is demonstrated that miR-206 could inhibit lipid accumulation and growth of HCC cells by targeting G6PD, suggesting that the mi R-206-G6PD axis may be a promising target for treating HCC.

Role of miRNA Sponges in Hepatocellular Carcinoma.



Long non-coding RNA LINC00673 promotes hepatocellular carcinoma progression and metastasis through negatively regulating miR-205.

Investigation of the role of lncRNA long intergenic noncoding RNA 00673 in tumorigenesis of HCC finds overexpression of LINC00673 promotes HCC cells progression by regulating miR-205, providing a prognostic biomarker and therapeutic target for HCC and is associated with poor survival of H CC patients.

Long noncoding RNA CASC2 regulates hepatocellular carcinoma cell oncogenesis through miR‐362‐5p/Nf‐κB axis

It is determined that CASC2 regulates HCC cell activity by targeting miR‐362‐5p and thus inhibiting the NF‐κB pathway and thus inhibit HCC growth and progression.

miR‐206 inhibits the growth of hepatocellular carcinoma cells via targeting CDK9

It is demonstrated that miR‐206 inhibited the growth of HCC cells through targeting CDK9, suggesting that the miR •206‐CDK9 pathway may be a novel target for the treatment of H CC.

Long non‐coding RNA CASC15 regulates gastric cancer cell proliferation, migration and epithelial mesenchymal transition by targeting CDKN1A and ZEB1

Functional experiments proved that the down‐ or up‐regulation of CASC15 inhibited or facilitated cell proliferation via the induction of cell cycle arrest and apoptosis, and also suppressed or accelerated cell migration and invasion by affecting the progression of the epithelial‐to‐mesenchymal transition (EMT).

MicroRNA-423 enhances the invasiveness of hepatocellular carcinoma via regulation of BRMS1.

Light is shed on miR-423 as a crucial factor that enhances HCC cell invasiveness, and suggested as a promising therapeutic target for HCC treatment.

Long non-coding RNA CASC15 is upregulated in hepatocellular carcinoma and facilitates hepatocarcinogenesis

CASC15 plays an important role in the progression of HCC, acting as an oncogene, suggesting that CASC15 may be a predictive biomarker of H CC.

miR-372 promotes breast cancer cell proliferation by directly targeting LATS2

It is demonstrated that miR-372 is frequently overexpressed in breast cancer cell lines and tissues and modulated the expression of large tumor suppressor kinase 2 (LATS2) by directly targeting its 3′-untranslated region in Breast cancer cells.

MicroRNA-495 suppresses cell proliferation and invasion of hepatocellular carcinoma by directly targeting insulin-like growth factor receptor-1.

Results provide novel insights into the molecular mechanism underlying HCC progression, and suggest that miR-495 may be investigated as a novel therapeutic target for patients with this disease.