MicroRNA-33a promotes cell proliferation and inhibits apoptosis by targeting PPARα in human hepatocellular carcinoma

Chang, Weiping; Zhang, Lei; Xian, Yuezhong; Yu, Zhaoxiang

doi:10.3892/etm.2017.4236

Cited by 25 publications

(15 citation statements)

References 34 publications

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“…It was demonstrated that miR-33a could promote cell growth by modulating the proliferation and apoptosis of HCC cells. Its direct target is PPARα, one of the targets of mTORC1[ 36 ].…”

Section: Mirnas In Hcc Molecular Pathwaysmentioning

confidence: 99%

Role of microRNAs in the main molecular pathways of hepatocellular carcinoma

Vasuri

Visani

Acquaviva

et al. 2018

WJG

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Hepatocellular carcinoma (HCC) is the most common primary liver malignant neoplasia. HCC is characterized by a poor prognosis. The need to find new molecular markers for its diagnosis and prognosis has led to a progressive increase in the number of scientific studies on this topic. MicroRNAs (miRNAs) are small non-coding RNA that play a role in almost all main cellular pathways. miRNAs are involved in the regulation of expression of the major tumor-related genes in carcinogenesis, acting as oncogenes or tumor suppressor genes. The aim of this review was to identify papers published in 2017 investigating the role of miRNAs in HCC tumorigenesis. miRNAs were classified according to their role in the main molecular pathways involved in HCC tumorigenesis: (1) mTOR; (2) Wnt; (3) JAK/STAT; (4) apoptosis; and (5) MAPK. The role of miRNAs in prognosis/response prediction was taken into consideration. Bearing in mind that the analysis of miRNAs in serum and other body fluids would be crucial for clinical management, the role of circulating miRNAs in HCC patients was also investigated. The most represented miRNA-regulated pathway in HCC is mTOR, but apoptosis, Wnt, JAK/STAT or MAPK pathways are also influenced by miRNA expression levels. These miRNAs could thus be used in clinical practice as diagnostic, prognostic or therapeutic targets for HCC treatment.

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“…It was demonstrated that miR-33a could promote cell growth by modulating the proliferation and apoptosis of HCC cells. Its direct target is PPARα, one of the targets of mTORC1[ 36 ].…”

Section: Mirnas In Hcc Molecular Pathwaysmentioning

confidence: 99%

Role of microRNAs in the main molecular pathways of hepatocellular carcinoma

Vasuri

Visani

Acquaviva

et al. 2018

WJG

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“…RNA was extracted and prepared for qRT-PCR as previously described (13). Total RNA was reverse-transcribed to cDNA with PrimeScript Reverse Transcriptase kit (Takara, Dalian, China) according to the manufacturer's protocol.…”

Section: Quantitative Real-time Polymerase Chain Reaction (Qrt-pcr)mentioning

confidence: 99%

microRNA‑196b promotes cell migration and invasion by targeting FOXP2 in hepatocellular carcinoma

Lin

Tian

et al. 2017

Oncol Rep

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Accumulating evidence indicates that microRNAs (miRNAs) play important roles in tumorigenesis and metastasis. Recent research has shown that miR‑196b is implicated in metastasis by regulating the migration and invasion of cancer cells. However, the clinical significance of miR‑196b and its role as well as the underlying mechanisms in hepatocellular carcinoma (HCC) remain largely unknown. Here, we detected miR‑196b expression in HCC and matched non-tumor tissues with qRT‑PCR. We found that miR‑196b displayed higher expression in HCC patient tissues and cells. Clinical analysis revealed that high miR‑196 expression was correlated with venous infiltration, advanced TNM stage and poor prognosis. Functionally, we demonstrated that miR‑196b promoted the migration and invasion of HCC cells in vitro. Moreover, miR‑196b knockdown restrained pulmonary metastasis in vivo. Mechanistically, we confirmed that miR‑196b could directly bind to 3'UTR of forkhead box P2 (FOXP2) mRNA and repress its expression. miR‑196b and FOXP2 showed a negative correlation in HCC tissues. More importantly, upregulation of FOXP2 antagonized miR‑196b‑mediated migration and invasion in Hep3B cells. Furthermore, FOXP2 knockdown partially reversed the anti‑metastatic function of the miR‑196b inhibitor on HCCLM3 cells. Taken together, we demonstrated that miR‑196b may function as a prognostic biomarker and suppressed FOXP2 expression, subsequently leading to the metastasis of HCC. Our findings highlight a novel mechanism of miR‑196b in the progression of HCC and identify miR‑196b/FOXP2 axis as a promising target for HCC.

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“…Chang et al found that miRNA-33a can promote Huh7 cell proliferation and inhibit apoptosis in vitro. The main target of this gene is PPARα (43). In addition, the Shah team found that activation of PPARα promoted HCC cell proliferation and induced hepatocarcinogenesis, and was associated with miRNA-let7C.…”

Section: Discussionmentioning

confidence: 99%

Knockdown expression of <i>MECR</i>, a novel gene of mitochondrial FAS II inhibits growth and colony-formation, promotes apoptosis of hepatocelluar carcinoma cells

Cai

Lin

Xiong

et al. 2019

BST

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Mitochondrial trans-2-enoyl-CoA reductase (MECR) is a protein-coding gene, and the protein encoded by this gene is an oxidoreductase that catalyzes the last step in mitochondrial fatty acid synthesis (mtFASII). Numerous studies have shown disorder of lipid metabolism is closely related with malignance, especially in liver cancer. Through pre-experiment, we found that the expression of MECR gene was highly expressed in hepatocelluar carcinoma (HCC) cell lines in vitro. This suggests that the MECR gene may play a role of oncogene in HCC. Therefore, we conducted a preliminary experimental study on the role of MECR gene in HCC cells in vitro. Objective to explore whether the MECR gene can affect the malignant biological behavior of HCC. We selected HCC cell line BEL-7404 as experimental cell, which involves the highest expression of MECR in the pre-experiment. We constructed MECR knockdwon lentivirus vector, and then infected HCC cell lines to down-regulate MECR expression, and establish negative control group (NC). Through various experiments of cytology, our study showed that knockdown of MECR inhibited cell proliferation and colony formation, promoted apoptosis, and inhibited metastasis in HCC cell lines BEL-7404. MECR might serve as a novel gene therapeutic target for the treatment of HCC. Further study is needed to elucidate the signaling pathway through which MECR functions in HCC.

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MicroRNA-33a promotes cell proliferation and inhibits apoptosis by targeting PPARα in human hepatocellular carcinoma

Cited by 25 publications

References 34 publications

Role of microRNAs in the main molecular pathways of hepatocellular carcinoma

Role of microRNAs in the main molecular pathways of hepatocellular carcinoma

microRNA‑196b promotes cell migration and invasion by targeting FOXP2 in hepatocellular carcinoma

Knockdown expression of <i>MECR</i>, a novel gene of mitochondrial FAS II inhibits growth and colony-formation, promotes apoptosis of hepatocelluar carcinoma cells

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