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Related Concept Videos

MicroRNAs01:22

MicroRNAs

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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Induced Pluripotent Stem Cells01:06

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Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
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mTOR Signaling and Cancer Progression03:03

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
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Decrease expression of microRNA-744 promotes cell proliferation by targeting c-Myc in human hepatocellular carcinoma.

Feng Lin1, Ruliang Ding1, Shuang Zheng1

  • 1Department of General Surgery, Taizhou First People's Hospital, Taizhou, Zhejiang Province 318020, P.R. China.

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|July 4, 2014
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MicroRNA 744 (miR-744) acts as a tumor suppressor in hepatocellular carcinoma (HCC) by inhibiting cell growth. Restoring miR-744 levels can reduce HCC proliferation by targeting c-Myc.

Keywords:
Cyclin D1Hepatocellular carcinoma (HCC)Tumor suppressorsc-MycmiR-744

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Area of Science:

  • Molecular Biology
  • Oncology
  • Gene Regulation

Background:

  • MicroRNAs (miRNAs) are key post-transcriptional regulators implicated in cancer.
  • miR-744 is frequently deregulated in various cancers, including hepatocellular carcinoma (HCC).
  • The precise role of miR-744 in HCC development is not fully understood.

Purpose of the Study:

  • To investigate the function of miR-744 in HCC tumor growth.
  • To determine the molecular mechanisms underlying miR-744's role in HCC.

Main Methods:

  • Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) for miR-744 expression.
  • Immunohistochemistry for c-Myc protein.
  • Cell proliferation and cell cycle assays.
  • Luciferase reporter assays to validate miR-744 targeting of c-Myc.

Main Results:

  • miR-744 expression was significantly downregulated in HCC tissues and cells.
  • Restoring miR-744 inhibited HCC cell proliferation and induced G1 cell cycle arrest.
  • c-Myc was identified as a direct target of miR-744.
  • Downregulation of miR-744 and upregulation of c-Myc were observed in HCC specimens.

Conclusions:

  • miR-744 functions as a tumor suppressor in HCC by targeting c-Myc.
  • Inhibition of HCC cell growth by miR-744 is mediated through c-Myc regulation.
  • miR-744 holds potential as a therapeutic target for miRNA-based HCC treatments.