Related Experiment Video

Updated: Mar 22, 2026

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells
09:45

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

Published on: May 21, 2019

9.0K

miR-33a is downregulated in melanoma cells and modulates cell proliferation by targeting PCTAIRE1

Fangzhen Tian1, Hongtu Wei2, Hua Tian3

  • 1Department of Dermatology, Jining No. 1 People's Hospital, Jining, Shandong 272000, P.R. China.

Oncology Letters
|April 14, 2016
PubMed

Insights

MicroRNA-33a (miR-33a) suppresses melanoma tumor growth by inhibiting cell proliferation and colony formation. It achieves this by downregulating PCTAIRE1, leading to increased p27 expression and tumor suppression.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biochemistry

Background:

  • MicroRNA-33a (miR-33a) is known to regulate lipid metabolism.
  • The function of miR-33a in cancer, particularly melanoma, remains largely unexplored.

Purpose of the Study:

  • To investigate the role of miR-33a in melanoma progression.
  • To elucidate the molecular mechanisms underlying miR-33a's function in melanoma cells.

Main Methods:

  • Quantitative real-time PCR to assess miR-33a and PCTAIRE1 expression.
  • Cell proliferation assays (colony formation, BrdU incorporation).
  • Western blotting for p27 and PCTAIRE1.
  • Luciferase reporter assay to confirm direct targeting of PCTAIRE1 by miR-33a.

Main Results:

  • miR-33a was significantly downregulated in melanoma cells compared to melanocytes.
  • Overexpression of miR-33a inhibited melanoma cell proliferation and colony formation.
  • miR-33a directly targets PCTAIRE1, suppressing its expression and leading to p27 accumulation.
  • PCTAIRE1 overexpression counteracted the tumor-suppressive effects of miR-33a.

Conclusions:

  • miR-33a functions as a tumor suppressor in melanoma.
  • The miR-33a/PCTAIRE1/p27 axis is a critical pathway in melanoma development.
  • These findings provide novel mechanistic insights into miR-33a's role in melanoma.
Keywords:
PCTAIRE1melanomamiR-33ap27

More Related Videos

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

8.1K
Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells06:09

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Published on: June 7, 2019

9.7K

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

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...
5.4K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
6.2K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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.
The mTOR pathway or the...
5.0K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
3.0K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
6.2K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
8.4K