Related Experiment Video

Updated: Dec 13, 2025

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

2.1K

MiR-182 affects renal cancer cell proliferation, apoptosis, and invasion by regulating PI3K/AKT/mTOR signaling

J-H Fu1, S Yang, C-J Nan

  • 1Department of Urology, Dongyang People's Hospital, Dongyang, Zhejiang, China.

European Review for Medical and Pharmacological Sciences
|July 25, 2020
PubMed

Insights

This article has been withdrawn due to suspected research misconduct. The publisher retracted the study on MiR-182's role in renal cancer after authors failed to verify data originality.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The PI3K/AKT/mTOR signaling pathway is crucial in cellular processes.
  • Dysregulation of this pathway is implicated in various cancers, including renal cancer.
  • MicroRNAs (miRNAs) are key regulators of gene expression and cellular functions.

Purpose of the Study:

  • To investigate the role of microRNA-182 (MiR-182) in renal cancer.
  • To determine how MiR-182 influences cancer cell proliferation, apoptosis, and invasion.
  • To elucidate the regulatory mechanism of MiR-182 on the PI3K/AKT/mTOR signaling pathway.

Main Methods:

  • Cell culture models of renal cancer were utilized.
  • MiR-182 expression levels were manipulated.
  • Assays were performed to assess cell proliferation, apoptosis, and invasion.
  • Western blotting was used to analyze the expression of proteins in the PI3K/AKT/mTOR pathway.

Main Results:

  • MiR-182 was found to affect renal cancer cell proliferation and apoptosis.
  • MiR-182 also impacted the invasive capabilities of renal cancer cells.
  • The study indicated that MiR-182 regulates the PI3K/AKT/mTOR signaling pathway.

Conclusions:

  • MiR-182 plays a significant role in the progression of renal cancer.
  • Targeting MiR-182 may offer a therapeutic strategy for renal cancer.
  • The PI3K/AKT/mTOR pathway is a key mediator of MiR-182's effects in renal cancer.

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

7.9K
Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma13:18

Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma

Published on: March 3, 2023

1.6K

Related Concept Videos

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...
4.5K
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...
5.0K
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...
5.0K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
7.0K
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.5K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
7.6K