KLF5 Cancer Research Results

KLF5, Krüppel-like factor 5: Click to Expand ⟱
Source:
Type:
KLF5 is a zinc finger transcription factor that plays crucial roles in regulating cell proliferation, differentiation, survival, migration, and angiogenesis.

– KLF5 is often overexpressed in certain subtypes and has been implicated in promoting cell proliferation and survival.

– Evidence suggests that high KLF5 levels can be associated with increased tumor aggressiveness and may contribute to resistance to therapy in some contexts.
Scientific Papers found: Click to Expand⟱
1860- dietFMD,  Chemo,    Fasting-mimicking diet blocks triple-negative breast cancer and cancer stem cell escape
- in-vitro, BC, SUM159 - in-vitro, BC, 4T1
PI3K↑, FMD activates PI3K-AKT, mTOR, and CDK4/6 as survival/growth pathways, which can be targeted by drugs to promote tumor regression.
Akt↑,
mTOR↑,
CDK4↑,
CDK6↑,
hyperG↓, FMD cycles also prevent hyperglycemia and other toxicities caused by these drugs.
TumCG↓, cycles of FMD significantly slowed down tumor growth, reduced tumor size, and caused an increased expression of intratumor Caspase3
TumVol↓,
Casp3↑,
BG↓, confirming our hypothesis that lowering intracellular glucose levels (through reduced extracellular levels or reduced uptake) reduces CSC survival
eff↑, 2DG potentiated the effect of FMD both in terms of delaying tumor progression and in decreasing the number of mammospheres derived by tumor masses,
eff∅, metformin did not show any additive or synergistic antitumor effect when combined with the FMD, thus suggesting that FMD and metformin have redundant effects on blood glucose levels
PKA↓, We have previously shown that prolonged fasting reduces the activity of protein kinase A (PKA) in different types of normal cells
KLF5↓, PKA inhibition resulted in the downregulation of KLF5, a potential therapeutic target for TNBC
p‑GSK‐3β↑, (GSK3β) phosphorylation
Nanog↓, stemness-associated genes NANOG and OCT4, and KLF2 and TBX3,
OCT4↓,
KLF2↓,
eff↑, Combining FMD cycles with PI3K/AKT/mTOR inhibitors results in long-term animal survival and reduces treatment-induced side effects
ROS↑, FMD resulted in an increased expression of pro-apoptotic molecules, such as BIM, and ASK1, a critical cellular stress sensor frequently activated by ROS, whose production was previously shown to be increased by the FMD
BIM↑,
ASK1↑,
PI3K↑, FMD cycles upregulate PI3K-AKT and mTOR pathways and downregulate CCNB-CDK1 while upregulating CCND-CDK4/6 signaling axes
Akt↑,
mTOR↑,
CDK1↓,
CDK4↑,
CDK6↑,
eff↑, combining STS with pictilisib, ipatasertib, and rapamycin, selective inhibitors for PI3K, AKT, and mTOR, respectively, resulted in enhanced cancer cell death and reduction of mammosphere numbers in SUM159 cells


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 ⓘ

hyperG↓, 1,   ROS↑, 1,  

Metal & Cofactor Biology ⓘ

KLF5↓, 1,  

Cell Death ⓘ

Akt↑, 2,   ASK1↑, 1,   BIM↑, 1,   Casp3↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK4↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

p‑GSK‐3β↑, 1,   mTOR↑, 2,   Nanog↓, 1,   OCT4↓, 1,   PI3K↑, 2,   TumCG↓, 1,  

Migration ⓘ

KLF2↓, 1,   PKA↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↑, 2,  

Drug Metabolism & Resistance ⓘ

eff↑, 3,   eff∅, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,  

Functional Outcomes ⓘ

TumVol↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: KLF5, Krüppel-like factor 5
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#:1195  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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