miR-139-5p Cancer Research Results

miR-139-5p, miR-139-5p: Click to Expand ⟱
Source:
Type: microRNA
miR-139-5p is a microRNA that plays a significant role in post-transcriptional regulation of gene expression.
-miR-139-5p often targets multiple genes involved in cell cycle regulation, apoptosis, migration, and invasion.

-Majority of studies across various cancer types suggest that lower expressions of miR-139-5p are correlated with more aggressive tumor behaviors and poorer prognoses.
Scientific Papers found: Click to Expand⟱
2047- Buty,    Sodium butyrate inhibits migration and induces AMPK-mTOR pathway-dependent autophagy and ROS-mediated apoptosis via the miR-139-5p/Bmi-1 axis in human bladder cancer cells
- in-vitro, CRC, T24/HTB-9 - in-vitro, Nor, SV-HUC-1 - in-vitro, Bladder, 5637 - in-vivo, NA, NA
HDAC↓, Sodium butyrate (NaB) is a histone deacetylase inhibitor and exerts remarkable antitumor effects in various cancer cells
AntiTum↑,
TumCMig↓, NaB inhibited migration
AMPK↑, induced AMPK/mTOR pathway-activated autophagy and reactive oxygen species (ROS) overproduction via the miR-139-5p/Bmi-1 axis
mTOR↑,
TumAuto↑,
ROS↑, NaB initiates ROS overproduction
miR-139-5p↑, NaB upregulates miR-139-5p and depletes Bmi-1 in bladder cancer cells
BMI1↓,
TumCI?, NaB significantly inhibited cell migration dose-dependently
E-cadherin↑, E-cadherin was markedly increased, while the expression of N-cadherin, Vimentin, and Snail was decreased
N-cadherin↓,
Vim↓,
Snail↓,
cl‑PARP↑, increased expression levels of cleaved PARP, cleaved caspase-3, and Bax and the concurrent decrease in Bcl-2 and Bcl-xl
cl‑Casp3↑,
BAX↑,
Bcl-2↓,
Bcl-xL↓,
MMP↓, impairs mitochondrial membrane potential
PINK1↑, activates the PINK1/ PARKIN pathway
PARK2↑,
TumMeta↓, NaB inhibits tumor metastasis and growth in vivo
TumCG↓,
LC3II↑, a significant increase in the levels of cleaved caspase3, p-AMPK, and LC3B-II along with decreased Bmi-1 and Vimentin
p62↓, elevated LC3B-II levels and degradation of p62
eff↓, NAC abolished the impairment of MMP and ROS overproduction. Interestingly, NAC also significantly inhibited apoptosis induced by NaB


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

PARK2↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   PINK1↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,  

Cell Death ⓘ

BAX↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   cl‑Casp3↑, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   p62↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

BMI1↓, 1,   HDAC↓, 1,   mTOR↑, 1,   TumCG↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   miR-139-5p↑, 1,   N-cadherin↓, 1,   Snail↓, 1,   TumCI?, 1,   TumCMig↓, 1,   TumMeta↓, 1,   Vim↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,  
Total Targets: 27

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: miR-139-5p, miR-139-5p
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1238  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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