Targeting c‐<scp>M</scp>et in Cancer by Micro<scp>RNA</scp>s: Potential Therapeutic Applications in Hepatocellular Carcinoma

Karagonlar, Zeynep Fırtına; Korhan, Peyda; Atabey, Neşe

doi:10.1002/ddr.21274

Cited by 21 publications

(15 citation statements)

References 102 publications

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“…Given that clinically targeting circadian gene or c-myc was either unsuccessful or impossible, this discovery is of great importance since there are many studies, including pre-clinical ones, testing the effect of miRNA inhibitors alone, or in combination with radiotherapy, chemotherapy, and immunotherapy in tumor treatment. 27 …”

Section: Discussionmentioning

confidence: 99%

miR-181d and c-myc-mediated inhibition of CRY2 and FBXL3 reprograms metabolism in colorectal cancer

et al. 2017

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Colorectal cancer (CRC) is the second major cause of tumor-related deaths. MicroRNAs (miRNAs) have pivotal roles in CRC progression. Here, we describe the effect of miR-181d on CRC cell metabolism and underlying molecular mechanism. Our data firmly demonstrated that knockdown of miR-181d suppressed CRC cell proliferation, migration, and invasion by impairing glycolysis. Mechanistically, miR-181d stabilized c-myc through directly targeting the 3′-UTRs of CRY2 and FBXL3, which subsequently increased the glucose consumption and the lactate production. Inhibition of c-myc via siRNA or small molecular inhibitor abolished the oncogenic effects of miR-181d on the growth and metastasis of CRC cells. Furthermore, c-myc/HDAC3 transcriptional suppressor complex was found to co-localize on the CRY2 and FBXL3 promoters, epigenetically inhibit their transcription, and finally induce their downregulation in CRC cells. In addition, miR-181d expression could be directly induced by an activation of c-myc signaling. Together, our data indicate an oncogenic role of miR-181d in CRC by promoting glycolysis, and miR-181d/CRY2/FBXL3/c-myc feedback loop might be a therapeutic target for patients with CRC.

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Section: Discussionmentioning

confidence: 99%

miR-181d and c-myc-mediated inhibition of CRY2 and FBXL3 reprograms metabolism in colorectal cancer

et al. 2017

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“…Previous studies have depicted the crucial role of miRNAs in hepatocarcinogenesis ( 14 , 28 ). miRNAs have been incorporated into a number of pathways to regulate cell proliferation, apoptosis, transdifferentiation and drug resistance.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of autophagy potentiates the proliferation inhibition activity of microRNA-7 in human hepatocellular carcinoma cells

Wang

Song

2017

Oncology Letters

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MicroRNAs (miRNAs/miRs) are important molecules that are able to regulate multiple cellular processes in cancer cells. miR-7 has been previously identified as a tumor suppressive miRNA in several types of cancer. The aim of the present study was to investigate whether miR-7 is able to regulate autophagy in hepatocellular carcinoma (HCC) cells. It was identified that miR-7 was significantly downregulated in tumor tissues compared with adjacent normal tissues. Overexpression of miR-7 inhibited cell proliferative activity, which was partially reversed by miR-7 inhibitor. In addition, overexpression of miR-7 significantly induced an increasen in autophagic activity, and luciferase activity assay and western blot analysis identified that mammalian target of rapamycin (mTOR) was a direct target of miR-7. In addition, inhibition of autophagy by 3-methyladenine resulted in a marked enhancement of the proliferation inhibition effect of miR-7. In conclusion, miR-7 was identified to induce proliferation inhibition and autophagy in HCC cells by targeting mTOR, and inhibition of autophagy may be utilized to enhance the antitumor activity of miR-7.

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“…With the development of genomics, miRNA expression profiles between tumor tissues and normal tissues could be rapidly established through high-throughput technologies such as gene chips, real-time PCR, etc. Dysregulation of miRNA expression has been confirmed in most tumors [ 19 , 20 ]. The up-regulated miRNAs in tumor cells are commonly considered to be oncogenic miRNAs (oncomiRs), which can silence the tumor suppressor genes.…”

Section: Mirnas and Cancermentioning

confidence: 99%

Targeting MicroRNAs in Cancer Gene Therapy

Sun

2017

Genes

154

100

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MicroRNAs (miRNAs) are a kind of conserved small non-coding RNAs that participate in regulating gene expression by targeting multiple molecules. Early studies have shown that the expression of miRNAs changes significantly in different tumor tissues and cancer cell lines. It is well acknowledged that such variation is involved in almost all biological processes, including cell proliferation, mobility, survival and differentiation. Increasing experimental data indicate that miRNA dysregulation is a biomarker of several pathological conditions including cancer, and that miRNA can exert a causal role, as oncogenes or tumor suppressor genes, in different steps of the tumorigenic process. Anticancer therapies based on miRNAs are currently being developed with a goal to improve outcomes of cancer treatment. In our present study, we review the function of miRNAs in tumorigenesis and development, and discuss the latest clinical applications and strategies of therapy targeting miRNAs in cancer.

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Targeting c‐Met in Cancer by MicroRNAs: Potential Therapeutic Applications in Hepatocellular Carcinoma

Cited by 21 publications

References 102 publications

miR-181d and c-myc-mediated inhibition of CRY2 and FBXL3 reprograms metabolism in colorectal cancer

miR-181d and c-myc-mediated inhibition of CRY2 and FBXL3 reprograms metabolism in colorectal cancer

Inhibition of autophagy potentiates the proliferation inhibition activity of microRNA-7 in human hepatocellular carcinoma cells

Targeting MicroRNAs in Cancer Gene Therapy

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