KCNN4 promotes invasion and metastasis through the MAPK/ERK pathway in hepatocellular carcinoma

Hepatocellular Carcinoma (HCC) is one of the most common malignancies in the world, and is well-known for its bad prognosis. Potassium calcium-activated channel subfamily N member 4 (KCNN4) is a type of intermediate conductance calcium-activated potassium channel, and increasing evidence suggests that KCNN4 contributes to the regulation of invasion and metastasis in a number of cancers. However, its clinical significance and biological function remain unclear in the HCC disease process. In this study, the expression levels of KCNN4 in 86 HCC samples were compared with corresponding paracancerous tissues. sh-RNA was used to reduce the expression of KCNN4 in Hep3B HCC cells in vitro; this was confirmed by Real time-PCR and western blotting. Wound healing, transwell assays and high content analysis were performed to investigate the tumor-promoting characteristics of KCNN4 in Hep3B HCC cells. As results, KCNN4 expression was significantly associated with preoperative serum alpha-fetoprotein level (p=0.038) and TNM stage (p=0.039). Additionally, patients with high KCNN4 amplification in HCC tissue exhibited shorter disease-free survival, whereas there was no statistical significance between KCNN4 amplification and overall survival. Wound healing and transwell assays showed that knockdown of KCNN4 expression could reduce migration and invasion abilities of HCC cells. High content analysis result showed that down-regulated KCNN4 could inhibit the ability of HCC cell proliferation. The mitogen-activated protein kinase (MAPK) pathway is active in cell proliferation, differentiation, migration, senescence, and apoptosis. Matrix metallopeptidase 9 and extracellular signal regulated kinase 1/2 (ERK1/2) were important biomarkers of MAPK/ERK pathway, knockdown of KCNN4 reduced the expression of MMP9 and ERK1/2. These findings showed that KCNN4 promotes HCC invasion and metastasis through the MAPK/ERK pathway.

Download Full-text

CircRNA LRIG3 knockdown inhibits hepatocellular carcinoma progression by regulating miR-223-3p and MAPK/ERK pathway

Archives of Medical Science ◽

10.5114/aoms/124975 ◽

2021 ◽

Author(s):

Hui Sun ◽

Junwei Zhai ◽

Li Zhang ◽

Yingnan Chen

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Proliferation ◽

Protein Kinase ◽

Molecular Mechanisms ◽

Mitogen Activated Protein Kinase ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Erk Pathway ◽

Mitogen Activated Protein ◽

Hcc Cells

IntroductionEmerging evidence suggests that circular RNAs (circRNAs) play critical roles in tumorigenesis. However, the roles and molecular mechanisms of circRNA leucine-rich repeat immunoglobulin domain-containing protein 3 (circ_LRIG3) in hepatocellular carcinoma (HCC) has not been investigated.Material and methodsThe expression levels of circ_LRIG3, miR-223-3p, and mitogen-activated protein kinase kinase 6 (MAP2K6) were determined by qRT-PCR. Flow cytometry was applied to determine the cell cycle distribution and apoptosis. Cell proliferation, migration and invasion were assessed by MTT, colony formation, and transwell assays. Western blot assay was employed to measure the protein levels of the snail, E-cadherin, MAP2K6, mitogen-activated protein kinase (MAPK), phospho-MAPK (p-MAPK), extracellular signal-regulated kinases (ERKs), and phospho-ERKs (p- ERKs). The relationship between miR-223-3p and circ_LRIG3 or MAP2K6 was predicted by bioinformatics tools and verified by dual-luciferase reporter assay. A xenograft tumor model was established to confirm the functions of circ_LRIG3 in vivo.ResultsCirc_LRIG3 and MAP2K6 expression were enhanced while miR-223-3p abundance was reduced in HCC tissues and cells. Knockdown of circ_LRIG3 inhibited cell proliferation, metastasis, and increasing apoptosis. MiR-223-3p was a target of circ_LRIG3, and its downregulation reversed the inhibitory effect of circ_LRIG3 knockdown on the progression of HCC cells. Moreover, MAP2K6 could bind to miR-223-3p, and MAP2K6 upregulation also abolished the suppressive impact of circ_LRIG3 interference on progression of HCC cells. Additionally, the silence of circ_LRIG3 suppressed the activation of the MAPK/ERK pathway and tumor growth by upregulating miR-223-3p and downregulating MAP2K6.ConclusionsCirc_LRIG3 knockdown inhibited HCC progression through regulating miR-223-3p/MAP2K6 axis and inactivating MAPK/ERK pathway.

Download Full-text

Kinesin family member 2C promotes hepatocellular carcinoma growth and metastasis via activating MEK/ERK pathway

Bioscience Biotechnology and Biochemistry ◽

10.1093/bbb/zbab154 ◽

2021 ◽

Author(s):

Qian Ding ◽

Caihua Jiang ◽

Yajing Zhou ◽

Jianping Duan ◽

Jianming Lai ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Proliferation ◽

Family Member ◽

Poor Prognosis ◽

Migration And Invasion ◽

Erk Pathway ◽

High Level ◽

The Impact ◽

Kinesin Family ◽

Hcc Cells

ABSTRACT The current work was intended to explore the function and mechanism of Kinesin family member 2C (KIF2C) in hepatocellular carcinoma (HCC). In this study, KIF2C expression was at a high level in HCC and indicated poor prognosis. Silencing KIF2C significantly suppressed the proliferation, migration and invasion in HCC cells. Furthermore, silencing KIF2C markedly decreased the expression of Snail, Vimentin, p-MEK and p-ERK, but increased E-cadherin expression in HCC cells. Moreover, we also found that MEK/ERK inhibitor U0126 could enhance the impact on cell proliferation, migration and invasion induced by silencing KIF2C in HCC. On the contrary, MEK/ERK activator PAF could weaken the impact induced by silencing KIF2C in HCC. Thus, our findings indicate that KIF2C can promote the proliferation, migration and invasion by activating MEK/ERK pathway in HCC.

Download Full-text

CircRNA LRIG3 knockdown inhibits the progression of hepatocellular carcinoma by regulating miR-223-3p/MAP2K6 axis and inactivating MAPK/ERK pathway

10.21203/rs.3.rs-17512/v1 ◽

2020 ◽

Author(s):

Hui Sun ◽

Junwei Zhai ◽

Li Zhang ◽

Yingnan Chen

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Proliferation ◽

Protein Kinase ◽

Mitogen Activated Protein Kinase ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Cell Cycle Distribution ◽

Erk Pathway ◽

Mitogen Activated Protein ◽

Hcc Cells

Abstract Background: Emerging evidence suggests that circular RNAs (circRNAs) play critical roles in tumorigenesis. However, the roles and molecular mechanism of circRNA leucine-rich repeat immunoglobulin domain-containing protein 3 (circ_LRIG3) in hepatocellular carcinoma (HCC) have not been investigated.Methods: The expression levels of circ_LRIG3, microRNA-223-3p (miR-223-3p), and mitogen-activated protein kinase kinase 6 (MAP2K6) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Flow cytometry was applied to determine the cell cycle distribution and cell apoptosis. Cell proliferation, migration and invasion were assessed by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay and transwell assay, respectively. Western blot assay was employed to measure the protein levels of snail, E-cadherin, MAP2K6, mitogen-activated protein kinase (MAPK), phospho-MAPK (p-MAPK), extracellular signal-regulated kinases (ERKs), and phospho-ERKs (p-ERKs). The relationship between miR-223-3p and circ_LRIG3 or MAP2K6 was predicted by bioinformatics tools and verified by dual-luciferase reporter assay. A xenograft tumor model was established to confirm the functions of circ_LRIG3 in vivo.Results: Circ_LRIG3 and MAP2K6 expression were enhanced while miR-223-3p abundance was reduced in HCC tissues and cells. Knockdown of circ_LRIG3 inhibited the progression of HCC cells via reducing cell proliferation, metastasis and increasing apoptosis. MiR-223-3p was a target of circ_LRIG3 and its downregulation reversed the inhibitory effect of circ_LRIG3 knockdown on progression of HCC cells. Moreover, MAP2K6 could bind to miR-223-3p, and MAP2K6 upregulation also abolished the suppressive impact of circ_LRIG3 interference on progression of HCC cells. Additionally, silence of circ_LRIG3 suppressed the activation of MAPK/ERK pathway and tumor growth by upregulating miR-223-3p and downregulating MAP2K6.Conclusion: Circ_LRIG3 knockdown inhibited HCC progression through regulating miR-223-3p/MAP2K6 axis and inactivating MAPK/ERK pathway, providing a potential therapeutic approach for patients with HCC.

Download Full-text

Circular RNA hsa_circ_101555 promotes hepatocellular carcinoma cell proliferation and migration by sponging miR-145-5p and regulating CDCA3 expression

Cell Death and Disease ◽

10.1038/s41419-021-03626-7 ◽

2021 ◽

Vol 12 (4) ◽

Author(s):

Xiaoguang Gu ◽

Jianan Zhang ◽

Yajuan Ran ◽

Hena Pan ◽

JinHong Jia ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Proliferation ◽

Biological Effects ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Casein Kinase 1 ◽

Mouse Xenograft Model ◽

Hcc Cells

AbstractCircular RNAs have been reported to play significant roles in regulating pathophysiological processes while also guiding clinical diagnosis and treatment of hepatocellular carcinoma (HCC). However, only a few circRNAs have been identified thus far. Herein, we investigated the role of a specific closed-loop structure of hsa_circ_101555 that was generated by back-splicing of the host gene casein kinase 1 gamma 1 (CSNK1G1) in the development and proliferation of HCC. We investigated the expression of Hsa_circ_101555 in HCC and normal tissues using bioinformatics. The expression level of hsa_circ_101555 was further detected by fluorescence in situ hybridization and qRT-PCR in ten HCC patients. Transwell, migration, WST-1 assays, and colony formation assays were used to evaluate the role of hsa_circ_101555 in HCC development and proliferation. The regulatory mechanisms of hsa_circ_101555 in miR-145-5p and CDCA3 were determined by dual luciferase reporter assay. A mouse xenograft model was also used to determine the effect of hsa_circ_101555 on HCC growth in vivo. hsa_circ_101555 showed greater stability than the linear RNA; while in vitro and in vivo results demonstrated that hsa_circ_101555 silencing significantly suppressed cell proliferation, migration, and invasion of HCC cells. Rescue experiments further demonstrated that suppression of miR-145-5p significantly attenuated the biological effects of hsa_circ_101555 knockdown in HCC cells. We also identified a putative oncogene CDCA3 as a potential miR-145-5p target. Thus, our results demonstrated that hsa_circ_101555 might function as a competing endogenous RNA of miR-145-5p to upregulate CDCA3 expression in HCC. These findings suggest that hsa_circ_101555 may be a potential therapeutic target for patients with HCC.

Download Full-text

LncRNA RHPN1-AS1 Promotes Cell Proliferation, Migration and Invasion Through Targeting miR-7-5p and Activating PI3K/AKT/mTOR Pathway in Hepatocellular Carcinoma

Technology in Cancer Research & Treatment ◽

10.1177/1533033820957023 ◽

2020 ◽

Vol 19 ◽

pp. 153303382095702

Author(s):

Xue-zhen Song ◽

Xiao-ning Ren ◽

Xiao-jun Xu ◽

Xiao-xuan Ruan ◽

Yi-li Wang ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Proliferation ◽

Molecular Mechanism ◽

Cancer Progression ◽

Cell Clone ◽

Mtor Pathway ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Gene Assay ◽

Hcc Cells

Hepatocellular carcinoma (HCC) is a severe disease with high mortality in the world. Emerging evidence has suggested that lncRNAs play an important role in cancer progression, including HCC. This study aimed to comprehensively investigate the effect of lncRNA RHPN1 antisense RNA 1 (RHPN1-AS1) on HCC and its underlying molecular mechanism. In this study, we evaluated the expressions of lncRNA RHPN1-AS1 and miR-7-5p by qRT-RCR in both HCC tissue and HCC cells. Our findings showed that lncRNA RHPN1-AS1 was upregulated in HCC tissue and HCC cells, while miR-7-5p was downregulated. LncRNA RHPN1-AS1 expression in HCC patients was closely related to vascular invasion, tumor-node-metastasis (TNM) stage and barcelona clinic liver cancer (BCLC) stage. Furthermore, we quantified cell clone-formation ability, proliferation, migration and invasion of HCCLM3 and MHCC97 H cells using several assays (colony formation assay, 5-Ethynyl-2′-deoxyuridine (EdU) assay and transwell assay, respectively). Functional experiments confirmed that silencing lncRNA RHPN1-AS1 inhibited cell proliferation, migration and invasion in HCCLM3 and MHCC97 H cells. After that, bioinformatics analysis, dual luciferase reporter gene assay, qRT-PCR and western blot were used to investigate the molecular mechanism of lncRNA RHPN1-AS1 on HCC. Mechanistically, the rescue experiments demonstrated that miR-7-5p inhibitor reversed the inhibition effect of silencing lncRNA RHPN1-AS1 on HCCLM3 cells proliferation, migration and invasion. Moreover, silencing lncRNA RHPN1-AS1 also inhibited the activation of PI3K/AKT/mTOR pathway. Taken together our findings demonstrated that lncRNA RHPN1-AS1 could facilitate cell proliferation, migration and invasion via targeting miR-7-5p and activating PI3K/AKT/mTOR pathway in HCC.

Download Full-text

Methionine Sulfoxide Reductase B1 Regulates Hepatocellular Carcinoma Cell Proliferation and Invasion via the Mitogen-Activated Protein Kinase Pathway and Epithelial-Mesenchymal Transition

Oxidative Medicine and Cellular Longevity ◽

10.1155/2018/5287971 ◽

2018 ◽

Vol 2018 ◽

pp. 1-15 ◽

Cited By ~ 8

Author(s):

Qiang He ◽

Hui Li ◽

Fanzhi Meng ◽

Xiangjun Sun ◽

Xu Feng ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Proliferation ◽

Epithelial Mesenchymal Transition ◽

Mapk Pathway ◽

Methionine Sulfoxide ◽

Methionine Sulfoxide Reductase ◽

Mitogen Activated Protein Kinase ◽

Migration And Invasion ◽

Mesenchymal Transition

Methionine sulfoxide reductase B1 (MsrB1) is a member of the selenoprotein family, which contributes to the reduction of methionine sulfoxides produced from reactive oxygen species (ROS) by redox processes in energy pathways. However, few studies have examined the role of MsrB1 in human hepatocellular carcinoma (HCC). We observed that MsrB1 is highly expressed in HCC tissues and that its expression correlated with the prognoses of patients with HCC after hepatectomy. In vitro, knockdown of MsrB1 inhibits HCC cell growth by MTT and EdU proliferation assay, and MsrB1 interference enhances H2O2/trx-induced apoptosis. We observed that phosphorylation of the key proteins of the MAPK pathway, namely, ERK, MEK, and p53, was inhibited, but PARP and caspase 3 were increased, thus infecting mitochondrial integrity. In vivo, MsrB1 knockdown effectively inhibited tumor growth. Furthermore, MsrB1 knockdown reduced HCC cell migration and invasion in a transwell assay through inhibition of cytoskeletal rearrangement and spread. This change was linked to epithelial-mesenchymal transition (EMT) inhibition resulting from increases in E-cadherin expression and decreases in expression in TGF-β1, Slug, MMP-2/9, and so on. MsrB1 regulates HCC cell proliferation and migration by modulating the MAPK pathway and EMT. Thus, MsrB1 may be a novel therapeutic target with respect to the treatment of HCC.

Download Full-text

MiR-18a-5p promotes proliferation, migration and invasion of hepatocellular carcinoma by targeting CPEB3

10.21203/rs.3.rs-39546/v1 ◽

2020 ◽

Author(s):

Jianxing Zheng ◽

Dongyang Wu ◽

Libing Wang ◽

Fengzhi Qu ◽

Daming Cheng ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Wound Healing ◽

Expression Profiles ◽

Bioinformatic Analysis ◽

Luciferase Assay ◽

Migration And Invasion ◽

Promoting Effect ◽

Migration Ability ◽

Qrt Pcr ◽

Hcc Cells

Abstract Objective The study aims to explore the mechanism of miR-18a-5p targeting CPEB3 gene in regulating the occurrence and development of hepatocellular carcinoma (HCC). Methods Differential and survival analyses were conducted on HCC expression profiles from TCGA database to screen out target miRNAs on which targeted prediction was conducted. qRT-PCR was used to detect the expressions of miR-18a-5p and CPEB3. MTT assay examined the proliferation activity, wound healing assay analyzed the migration ability and Transwell assay detected the invasion ability of HCC cells after overexpressing miR-18a-5p.Dual luciferase assay verified the targeting relationship between miR-18a-5p and CPEB3. Meanwhile, MTT, wound healing and Transwellassays determined whether the overexpression of CPEB3 reversed the promoting effect of miR-18a-5p on HCC cells. Results Bioinformatic analysis showed that miR-18a-5p was significantly highly expressed in HCC tissues and its target binding site was found in CPEB3 genewith low expression.The qRT-PCR found that high miR-18a-5p expression was observed in HCC cells, and the expression of CPEB3 was significantly low. Overexpression of miR-18a-5p promoted proliferation, migration and invasion of HCC cells. Dual luciferase assay observed that miR-18a-5p inhibited the expression of CPEB3 while overexpression of CPEB3 reversed the promoting effect of miR-18a-5p on the growth of HCCcells. Conclusion miR-18a-5p promoted the proliferation and migration of HCC cells by inhibiting the expression of CPEB3. The role of miR-18a-5p /CPEB3 in HCCfound in this study provided a new potential target for the prognostic treatment of HCC patients.

Download Full-text

Total flavonoids of Radix Tetrastigma suppress inflammation-related hepatocellular carcinoma cell metastasis

Molecular Genetics and Genomics ◽

10.1007/s00438-020-01759-6 ◽

2021 ◽

Author(s):

Zhendong Liu ◽

Fangmi Ding ◽

Xingyong Shen

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Proliferation ◽

Cell Migration ◽

Inhibitory Effect ◽

Migration And Invasion ◽

Total Flavonoids ◽

Cell Migration And Invasion ◽

Proinflammatory Mediators ◽

Cox 2 ◽

Hcc Cells

AbstractThis study aimed to investigate the effects of the total flavonoids of Radix Tetrastigma (RTF) on inflammation-related hepatocellular carcinoma (HCC) development. Extracted RTF was diluted to different concentrations for subsequent experiments. HCC cells were cotreated with lipopolysaccharide (LPS) and RTF to investigate the effects of RTF on LPS-stimulated HCC cells. A CCK-8 kit was used to measure cell proliferation. Apoptosis was detected with a flow cytometer. Cell migration and invasion were quantified by wound healing and Transwell assays, respectively. The expression of TLR4 and COX-2 and activation of the NF-κB pathway were determined by Western blotting. Treatment with LPS significantly enhanced cell proliferation and decreased the apoptosis rate, while cell migration and invasion were notably upregulated. RTF suppressed the proliferation and invasion induced by LPS stimulation and promoted HCC cell apoptosis. The protein levels of Bax and cleaved caspase-3 were decreased and that of Bcl-2 was increased by LPS in HCC cells, which could be rescued by RTF. RTF significantly inhibited the LPS-induced expression of the proinflammatory mediators IL-6 and IL-8 in HCC cells. Mechanistically, with RTF treatment, the upregulated expression of TLR4 and COX-2 induced by LPS was obviously downregulated. Furthermore, the phosphorylation of NF-κB/p65 was significantly decreased in LPS-stimulated cells after supplementation with RTF. Our study suggests that RTF exerts a significant inhibitory effect on the LPS-induced enhancement of the malignant behaviors of HCC cells via inactivation of TLR4/NF-κB signaling. RTF may be a promising chemotherapeutic agent to limit HCC development and inflammation-mediated metastasis.

Download Full-text

DEAH-box polypeptide 32 promotes hepatocellular carcinoma progression via activating the β-catenin pathway

10.21203/rs.3.rs-27420/v1 ◽

2020 ◽

Author(s):

Xiaoyun Hu ◽

Guosheng Yuan ◽

Qi Li ◽

Jing Huang ◽

Xiao Cheng ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Proliferation ◽

Tumor Growth ◽

Ectopic Expression ◽

Migration And Invasion ◽

High Morbidity ◽

Rt Pcr ◽

Mesenchymal Transition ◽

Potential Biomarker ◽

Hcc Cells

Abstract Background Hepatocellular carcinoma (HCC) is a refractory cancer with high morbidity and high mortality. It has been reported that DEAH-box polypeptide 32 (DHX32) was upregulated in several types of malignancies and predicted poor prognosis, which was associated with tumor growth and metastasis. However, the expression of DHX32 in HCC and its role in HCC progression remain largely unknown. Methods Western blot and RT-PCR assays were used to detect the expression of DHX32 and epithelial mesenchymal transition (EMT)-related genes in HCC cells. Wound-healing and Transwell invasion assays were performed to determine the effect of DHX32 and β-catenin on the migration and invasion of HCC cells. Cell proliferation was examined by EdU cell proliferation assay. Results In our study, we found that high level of DHX32 expression was associated with reduced overall survival in HCC patients. DHX32 expression was upregulated in human HCC cells and ectopic expression of DHX32 induced EMT, promoted the migration, invasion, and proliferation of HCC cells, and enhanced tumor growth. Silencing DHX32 reversed EMT, inhibited the migration, invasion, and proliferation of HCC cells, and suppressed tumor growth. RT-PCR assay revealed that DHX32 regulated the expression of CTNNB1, CCND1, COX2, MMP7, and WIF1 in HCC cells. Mechanistic investigations showed that silencing DHX32 decreased the expression of β-catenin in nucleus and β-catenin siRNA abrogated DHX32-mediated EMT, migration, invasion, and proliferation in HCC cells. Conclusions Our data suggested that DHX32 was an attractive regulator of HCC progression and indicated DHX32 can serve as a potential biomarker and therapeutic target for HCC patients.

Download Full-text

MiR-3144 Suppresses Cell Proliferation, Migration, Invasion and Promotes Cell Apoptosis by Targeting Steap4 in Hepatocellular Carcinoma

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2019.2114 ◽

2019 ◽

Vol 9 (8) ◽

pp. 1100-1107

Author(s):

Qiuyuan Shi ◽

Dandan Shen ◽

Yuanjiang Shang

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Proliferation ◽

Cell Lines ◽

Cell Apoptosis ◽

Apoptotic Cell ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Invasion And Migration ◽

Novel Target ◽

Hcc Cells

Background: MicroRNAs (miRNAs) play important roles in the carcinogenesis and progression of hepatocellular carcinoma (HCC). Previous studies have shown that miR-3144 is down-regulated in HCC tissues. The present study investigated the expression and biological roles, underlying mechanisms of miR-3144 in HCC cell lines. Methods and material: RT-qPCR analysis was performed to detect miR-3144 expression in the HCC cell lines and normal hepatic cell line. CCK-8 assay showed that the effect of miR-3144 expression on cell proliferation. Using wound healing assay and Transwell assay to detect the effect of miR-3144 on cell invasion and migration of HCC. Flow cytometry assay showed that miR-3144 induced apoptotic cell death in the SK-HEP-1 cells. Luciferase reporter assay was performed to evaluate the interaction between miR-3144 and the Steap4 3′-UTR. Western blotting assay were performed to investigate the effect of miR-3144 expression on the expression of CDK2, cyclinE1, p21, MMP2, MMP9 and Steap4. Results: MiR-3144 expression was downregulated in HCC cell lines. MiR-3144 overexpression inhibited the proliferation of HCC cells via regulating CDK2, cyclinE1 and p21 in SK-HEP-1 cells. MiR-3144 suppressed the migration and invasion of HCC cells via decreasing the MMP2 and MMP9. Further, miR-3144 promotes cell apoptosis of HCC. Moreover, miR-3144 negatively regulated Steap4 expression by directly binding to the 3′-UTR of Steap4 mRNA. Conclusion: Our results suggested that miR-3144 may be a novel target for future HCC therapy.

Download Full-text