miR-155 Cancer Research Results

miR-155, miR-155: Click to Expand ⟱
Source:
Type: Onco-microRNA
miR-155 has been found to be overexpressed in various types of cancer, including breast, lung, colon, and lymphoma. This overexpression has been associated with cancer progression, metastasis, and poor prognosis.
Scientific Papers found: Click to Expand⟱
4707- CUR,    The Potential Role of Curcumin as a Regulator of microRNA in Colorectal Cancer: A Systematic Review
- Review, Var, NA
miR-497↑, Curcumin was found to cause the upregulation of miR-497, miR-200c, miR-200b, miR-409-3p, miR‐34, miR‐126, miR-145, miR-206, miR-491, miR-141, miR-429, miR-101, and miR-15a
miR-200c↑,
miR-409-3p↑,
miR-34a↑,
miR-126↑,
miR-145↑,
miR-206↑,
miR-491↑,
miR-141↑,
miR-429↑,
miR-101↑,
miR-15↑,
miR-21↓, and the downregulation of miR-21, miR-155, miR‐221, miR‐222, miR-17-5p, miR-130a, miR-27, and miR-20a.
miR-155↓,
miR-221↓,
miR‐222↓,
miR-17↓,
miR-130a↓,
miR-27a-3p↓,
miR-20↓,

3069- RES,    Resveratrol Inhibits NLRP3 Inflammasome-Induced Pyroptosis and miR-155 Expression in Microglia Through Sirt1/AMPK Pathway
- in-vitro, Nor, N9
*antiOx↑, antioxidant, anti-carcinogenic, anti-obesity, anti-aging, anti-inflammatory, immunomodulatory properties.
*Inflam↓,
*ROS↓, Our results demonstrated that resveratrol inhibits LPS- and ATP-activated NLRP3 inflammasome and protects microglial cells upon oxidative stress, proinflammatory cytokine production, and pyroptotic cell death resulting from inflammasome activation.
*NF-kB↓, resveratrol inhibits nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling and activates AMPK/Sirt1 pathways.
*AMPK↑,
*SIRT1↑,
*miR-155↓, Furthermore, our results indicated that resveratrol downregulated inflammasome-induced miR-155 expression
*NLRP3↓, To sum up, our results suggest that resveratrol suppresses the NLRP3 inflammasome and miR-155 expression through AMPK and Sirt1 pathways in microglia.

1748- RosA,    The Role of Rosmarinic Acid in Cancer Prevention and Therapy: Mechanisms of Antioxidant and Anticancer Activity
- Review, Var, NA
AntiCan↑, RA exhibits significant potential as a natural agent for cancer prevention and treatment
*BioAv↝, Various factors, including its lipophilic nature, stability in the gastrointestinal tract, and interactions with food, can significantly influence its absorption
*CardioT↓, RA attenuated these effects by reducing ROS levels, indicating its potential role as a cardioprotective agent during chemotherapy.
*Iron↓, Another significant mechanism antioxidant activity of RA is its capacity to chelate transition metal ions, particularly iron (Fe2+) and copper (Cu2+), which can catalyze the formation of highly reactive hydroxyl radicals through the Fenton reaction.
*ROS↓, forming stable complexes with Fe2+ and Cu2+, thus inhibiting their pro-oxidant activity.
*SOD↑, SOD, CAT, and GPx, play crucial roles in neutralizing ROS and maintaining cellular redox homeostasis. RA upregulates the expression and activity of these enzymes
*Catalase↑,
*GPx↑,
*NRF2↑, activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, a primary regulator of the antioxidant response
MARK4↓, Anwar’s study demonstrated that RA inhibited MARK4 activity in MDA-MB-231 breast cancer cells, resulting in dose-dependent apoptosis
MMP9↓, RA effectively inhibited cancer cell invasion and migration by reducing matrix metalloproteinase-9 (MMP-9) activity
TumCCA↑, caused cell cycle arrest
Bcl-2↓, RA downregulates Bcl-2 expression and upregulates Bax, thereby promoting apoptosis
BAX↑,
Apoptosis↑,
E-cadherin↑, promoting E-cadherin expression, while downregulating N-cadherin and vimentin
N-cadherin↓,
Vim↓,
Gli1↓, induced apoptosis by downregulating Gli1, a key component of the Hedgehog signaling pathway,
HDAC2↓, RA induced apoptosis by modulating histone deacetylase 2 (HDAC2) expression
Warburg↓, anti-Warburg effect of RA in colorectal carcinoma
Hif1a↓, RA inhibits hypoxia-inducible factor-1 alpha (HIF-1α) and downregulates miR-155
miR-155↓,
p‑PI3K↑, RA has been shown to upregulate p-PI3K, protecting cells through the PI3K/Akt pathway,
ROS↑, RA, induces significant ROS generation in A549 cells, which triggers both apoptosis and autophagy.
*IronCh↑, RA’s dual nature as both a phenolic acid and a flavonoid-related compound enables it to chelate metal ions and prevent the formation of free radicals,

3036- RosA,    Anti-Warburg effect of rosmarinic acid via miR-155 in colorectal carcinoma cells
- in-vitro, CRC, HCT8 - in-vitro, CRC, HCT116 - in-vitro, CRC, LS174T
GlucoseCon↓, RA suppressed glucose consumption and lactate generation in colorectal carcinoma cells;
lactateProd↓,
Hif1a↓, RA inhibited the expression of transcription factor hypoxia-inducible factor-1α (HIF-1α) that affects the glycolytic pathway.
Inflam↓, RA could not only repress proinflammatory cytokines using enzyme-linked immunosorbent assay but it could also suppress microRNAs related to inflammation by real-time PCR
miR-155↓, MiR-155 induces the Warburg effect and is reversed by RA
STAT3↓, RA could inhibit the expression of transcription factor STAT3, and it suppressed the phosphorylation of STAT3
Glycolysis↓, Meanwhile, RA inhibited the expression of transcription factor HIF-1α that affected the glycolytic pathway
IL6↓, RA could significantly regulate miR-155 and in turn alter the IL-6/STAT3 signaling, resulting in the inhibition of inflammation in the tumor micro environment and the eventual anti-Warburg effect
Warburg↓,

1437- SFN,    Dietary Sulforaphane in Cancer Chemoprevention: The Role of Epigenetic Regulation and HDAC Inhibition
- Review, NA, NA
HDAC↓, 15 μM
HDAC1↓,
HDAC2↓,
HDAC3↓,
HDAC8↓,
eff↑, this evidence suggests that sulforaphane may also compromise DNA repair mechanisms in cancer cells with selectivity.
ac‑HSP90↑,
DNMT1↓, 10 μM sulforaphane in 6 days inhibited DNMT1 and DNMT3a expression by 48% and 78%, respectively
DNMT3A↓,
hTERT/TERT↓,
NRF2↑, enhance nuclear translocation of Nrf2 and increase expression of Nrf2-target antioxidant genes, including HO-1, NQO1, and UGT1A1
HO-1↑,
NQO1↑,
miR-155↓,
miR-200c↑,
SOX9↓,
*toxicity↓, broccoli sprout-infused beverage containing 400 μM glucoraphanin nightly for 2 weeks causing no adverse effects and being well tolerated in 200 subjects

978- SIL,    A comprehensive evaluation of the therapeutic potential of silibinin: a ray of hope in cancer treatment
- Review, NA, NA
PI3K↓,
Akt↓,
NF-kB↓,
Wnt/(β-catenin)↓,
MAPK↓,
TumCP↓,
TumCCA↑, G0/G1 cell cycle arrest
Apoptosis↑, In T24 and UM-UC-3 human bladder cancer cells, silibinin treatment at a concentration of 10 μM significantly inhibited proliferation, migration, invasion, and induced apoptosis.
p‑EGFR↓,
JAK2↓,
STAT5↓,
cycD1/CCND1↓,
hTERT/TERT↓,
AP-1↓,
MMP9↓,
miR-21↓,
miR-155↓,
Casp9↑,
BID↑,
ERK↓, ERK1/2
Akt2↓,
DNMT1↓,
P53↑,
survivin↓,
Casp3↑,
ROS↑, cytotoxicity of silibinin in Hep-2 cells was associated with the accumulation of intracellular reactive oxygen species (ROS), which could be mitigated by the ROS scavenger NAC.

2212- SK,    Shikonin Exerts an Antileukemia Effect against FLT3-ITD Mutated Acute Myeloid Leukemia Cells via Targeting FLT3 and Its Downstream Pathways
- in-vitro, AML, NA
FLT3↓, SHK suppresses the expression and phosphorylation of FLT3 receptors and their downstream molecules
NF-kB↓, Inhibition of the NF-κB/miR-155 pathway is an important mechanism through which SHK kills FLT3-AML cells
miR-155↓,
Diff↑, Moreover, a low concentration of SHK promotes the differentiation of AML cells with FLT3-ITD mutations.
TumCG↓, Finally, SHK could significantly inhibit the growth of MV4-11 cells in leukemia bearing mice.


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↑, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↑, 2,  

Core Metabolism/Glycolysis ⓘ

GlucoseCon↓, 1,   Glycolysis↓, 1,   lactateProd↓, 1,   Warburg↓, 2,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,   BID↑, 1,   Casp3↑, 1,   Casp9↑, 1,   hTERT/TERT↓, 2,   MAPK↓, 1,   miR-497↑, 1,   survivin↓, 1,  

Kinase & Signal Transduction ⓘ

SOX9↓, 1,  

Transcription & Epigenetics ⓘ

miR-145↑, 1,   miR-21↓, 2,   miR-27a-3p↓, 1,   miR-409-3p↑, 1,  

Protein Folding & ER Stress ⓘ

ac‑HSP90↑, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 2,   DNMT3A↓, 1,   P53↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,   ERK↓, 1,   FLT3↓, 1,   Gli1↓, 1,   HDAC↓, 1,   HDAC1↓, 1,   HDAC2↓, 2,   HDAC3↓, 1,   HDAC8↓, 1,   miR-101↑, 1,   miR-34a↑, 1,   miR-429↑, 1,   PI3K↓, 1,   p‑PI3K↑, 1,   STAT3↓, 1,   STAT5↓, 1,   TumCG↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

Akt2↓, 1,   AP-1↓, 1,   E-cadherin↑, 1,   MARK4↓, 1,   miR-130a↓, 1,   miR-141↑, 1,   miR-155↓, 6,   miR-20↓, 1,   miR-200c↑, 2,   miR-206↑, 1,   miR-221↓, 1,   miR-491↑, 1,   miR‐222↓, 1,   MMP9↓, 2,   N-cadherin↓, 1,   TumCP↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

p‑EGFR↓, 1,   Hif1a↓, 2,   miR-126↑, 1,   miR-15↑, 1,   miR-17↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL6↓, 1,   Inflam↓, 1,   JAK2↓, 1,   NF-kB↓, 2,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Clinical Biomarkers ⓘ

p‑EGFR↓, 1,   hTERT/TERT↓, 2,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,  
Total Targets: 79

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   Iron↓, 1,   NRF2↑, 1,   ROS↓, 2,   SOD↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   SIRT1↑, 1,  

Migration ⓘ

miR-155↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,  

Functional Outcomes ⓘ

CardioT↓, 1,   toxicity↓, 1,  
Total Targets: 17

Scientific Paper Hit Count for: miR-155, miR-155
2 Rosmarinic acid
1 Curcumin
1 Resveratrol
1 Sulforaphane (mainly Broccoli)
1 Silymarin (Milk Thistle) silibinin
1 Shikonin
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#:763  State#:%  Dir#:1
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