miR-27a-3p Cancer Research Results

miR-27a-3p, miR-27a-3p: Click to Expand ⟱
Source:
Type: oncogenic miRNA
miR-27a-3p is often found to be upregulated. It can promote tumor growth and metastasis by targeting and downregulating tumor suppressor genes.
Scientific Papers found: Click to Expand⟱
1426- Bos,  CUR,  Chemo,    Novel evidence for curcumin and boswellic acid induced chemoprevention through regulation of miR-34a and miR-27a in colorectal cancer
- in-vivo, CRC, NA - in-vitro, CRC, HCT116 - in-vitro, CRC, RKO - in-vitro, CRC, SW480 - in-vitro, RCC, SW-620 - in-vitro, RCC, HT-29 - in-vitro, CRC, Caco-2
miR-34a↑, curcumin and AKBA induced upregulation of tumor-suppressive miR-34a and downregulation of miR-27a in CRC cells
miR-27a-3p↓,
TumCG↓,
BAX↑,
Bcl-2↓,
PARP1↓,
TumCCA↑,
Apoptosis↑,
cMyc↓,
CDK4↓,
CDK6↓,
cycD1/CCND1↓,
ChemoSen↑, combined treatment further increased the inhibitory effects
miR-34a↑, miR-34a expression was upregulated by curcumin and further elevated by concurrent treatment with curcumin and AKBA in HCT116 cell
miR-27a-3p↓,

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↓,

4708- CUR,    Molecular mechanisms underlying curcumin-mediated microRNA regulation in carcinogenesis; Focused on gastrointestinal cancers
- Review, GC, NA
chemoPv↑, Curcumin is well known for its chemopreventive and anti-cancer properties.
AntiCan↑,
*antiOx↑, Mechanistically, curcumin exerts its biological impacts via antioxidant and anti-inflammatory effects through the interaction with various transcription factors and signaling molecules.
*Inflam↓,
miR-21↓, Table 1
miR-34a↑,
miR-200b↑,
miR-27a-3p↓,

2688- CUR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Var, NA - Review, AD, NA
*ROS↓, CUR reduced the production of ROS
*SOD↑, CUR also upregulated the expression of superoxide dismutase (SOD) genes
p16↑, The effects of CUR on gene expression in cancer-associated fibroblasts obtained from breast cancer patients has been examined. CUR increased the expression of the p16INK4A and other tumor suppressor proteins
JAK2↓, CUR decreased the activity of the JAK2/STAT3 pathway
STAT3↓,
CXCL12↓, and many molecules involved in cellular growth and metastasis including: stromal cell-derived factor-1 (SDF-1), IL-6, MMP2, MMP9 and TGF-beta
IL6↓,
MMP2↓,
MMP9↓,
TGF-β↓,
α-SMA↓, These effects reduced the levels of alpha-smooth muscle actin (alpha-SMA) which was attributed to decreased migration and invasion of the cells.
LAMs↓, CUR suppressed Lamin B1 and
DNAdam↑, induced DNA damage-independent senescence in proliferating but not quiescent breast stromal fibroblasts in a p16INK4A-dependent manner.
*memory↑, CUR has recently been shown to suppress memory decline by suppressing beta-site amyloid precursor protein cleaving enzyme 1 (BACE1= Beta-secretase 1, an important gene in AD) expression which is implicated in beta-amyoid pathology in 5xFAD transgenic
*cognitive↑, CUR was found to decrease adiposity and improve cognitive function in a similar fashion as CR in 15-month-old mice.
*Inflam↓, The effects of CUR and CR were positively linked with anti-inflammatory or antioxidant actions
*antiOx↑,
*NO↑, CUR treatment increased nNOS expression, acidity and NO concentration
*MDA↓, CUR treatment resulted in decreased levels of MDA
*ROS↓, CUR treatment was determined to cause reduction of ROS in the AMD-RPEs and protected the cells from H2O2-induced cell death by reduction of ROS levels.
DNMT1↓, CUR has been shown to downregulate the expression of DNA methyl transferase I (DNMT1)
ROS↑, induction of ROS and caspase-3-mediated apoptosis
Casp3↑,
Apoptosis↑,
miR-21↓, CUR was determined to decrease both miR-21 and anti-apoptotic protein expression.
LC3II↓, CUR also induced proteins associated with cell death such as LC3-II and other proteins in U251 cells
ChemoSen↑, The combined CUR and temozolomide treatment resulted in enhanced toxicity in U-87 glioblastoma cells.
NF-kB↓, suppression of NF-kappaB activity
CSCs↓, Dendrosomal curcumin increased the expression of miR-145 and decreased the expression of stemness genes including: NANOG, OCT4A, OCT4B1, and SOX2 [113]
Nanog↓,
OCT4↓,
SOX2↓,
eff↑, A synergistic interaction was observed when emodin and CUR were combined in terms of inhibition of cell growth, survival and invasion.
Sp1/3/4↓, CUR inducing ROS which results in suppression of specificity protein expression (SP1, SP3 and SP4) as well as miR-27a.
miR-27a-3p↓,
ZBTB10↑, downregulation of miR-27a by CUR, increased expression of ZBTB10 occurred
SOX9?, This resulted in decreased SOX9 expression.
ChemoSen↑, CUR used in combination with cisplatin resulted in a synergistic cytotoxic effect, while the effects were additive or sub-additive in combination with doxorubicin
VEGF↓, Some of the effects of CUR treatment are inhibition of NF-κB activity and downstream effector proteins, including: VEGF, MMP-9, XIAP, BCL-2 and Cyclin-D1.
XIAP↓,
Bcl-2↓,
cycD1/CCND1↓,
BioAv↑, Piperine is an alkaloid found in the seeds of black pepper (Piper nigrum) and is known to enhance the bioavailability of several therapeutic agents, including CUR
Hif1a↓, CUR inhibits HIF-1 in certain HCC cell lines and in vivo studies with tumor xenografts. CUR also inhibited EMT by suppressing HIF-1alpha activity in HepG2 cells
EMT↓,
BioAv↓, CUR has a poor solubility in aqueous enviroment, and consequently it has a low bioavailability and therefore low concentrations at the target sites.
PTEN↑, CUR treatment has been shown to result in activation of PTEN, which is a target of miR-21.
VEGF↓, CUR treatment resulted in a decrease of VEGF and activated Akt.
Akt↑,
EZH2↓, CUR also suppressed EZH2 expression by induction of miR-let 7c and miR-101.
NOTCH1↓, The expression of NOTCH1 was inhibited upon EZH2 suppression [
TP53↑, CUR has been shown to activate the TP53/miR-192-5p/miR-215/XIAP pathway in NSCLC.
NQO1↑, CUR can also induce the demethylation of the nuclear factor erythroid-2 (NF-E2) related factor-2 (NRT2) gene which in turn activates (NQO1), heme oxygenase-1 (HO1) and an antioxidant stress pathway which can prevent growth in mouse TRAMP-C1 prostate
HO-1↑,

104- RES,  QC,    Resveratrol and Quercetin in Combination Have Anticancer Activity in Colon Cancer Cells and Repress Oncogenic microRNA-27a
- in-vitro, Colon, HT-29
Casp3↑, RQ also induced caspase-3-cleavage (2-fold) and increased PARP cleavage.
PARP↑,
survivin↓, RQ also decreased expression of survivin protein
miR-27a-3p↓, RQ decreased microRNA-27a (miR-27a) and induced zinc finger protein ZBTB10
Sp1/3/4↓, RQ treatment decreased the expression of Sp1, Sp3, and Sp4 mRNA and this was accompanied by decreased protein expression
ZBTB10↑,
ROS⇅, RQ slightly induced the generation of ROS at low concentrations (0–10 μg/mL) whereas at concentrations higher than 20 μg/mL generation of ROS was significantly reduced
TAC↑, RQ decreased the generation of reactive oxygen species (ROS) by up to 2.25-fold and increased the antioxidant capacity by up to 3-fold in HT-29 cells (3.8-60 μg/mL)
tumCV↓, HT-29 cell viability (Fig. 2A) was significantly decreased by RQ in a dose- and time-dependent manner


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↑, 1,   NQO1↑, 1,   ROS↑, 1,   ROS⇅, 1,   TAC↑, 1,  

Mitochondria & Bioenergetics ⓘ

XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,  

Cell Death ⓘ

Akt↑, 1,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 2,   Casp3↑, 2,   miR-497↑, 1,   survivin↓, 1,  

Kinase & Signal Transduction ⓘ

SOX9?, 1,   Sp1/3/4↓, 2,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   miR-145↑, 1,   miR-21↓, 3,   miR-27a-3p↓, 6,   miR-409-3p↑, 1,   tumCV↓, 1,  

Autophagy & Lysosomes ⓘ

LC3II↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMT1↓, 1,   p16↑, 1,   PARP↑, 1,   PARP1↓, 1,   TP53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 2,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 1,   miR-101↑, 1,   miR-34a↑, 4,   miR-429↑, 1,   Nanog↓, 1,   NOTCH1↓, 1,   OCT4↓, 1,   PTEN↑, 1,   SOX2↓, 1,   STAT3↓, 1,   TumCG↓, 1,  

Migration ⓘ

CXCL12↓, 1,   LAMs↓, 1,   miR-130a↓, 1,   miR-141↑, 1,   miR-155↓, 1,   miR-20↓, 1,   miR-200b↑, 1,   miR-200c↑, 1,   miR-206↑, 1,   miR-221↓, 1,   miR-491↑, 1,   miR‐222↓, 1,   MMP2↓, 1,   MMP9↓, 1,   TGF-β↓, 1,   α-SMA↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,   miR-126↑, 1,   miR-15↑, 1,   miR-17↓, 1,   VEGF↓, 2,   ZBTB10↑, 2,  

Immune & Inflammatory Signaling ⓘ

IL6↓, 1,   JAK2↓, 1,   NF-kB↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 3,   eff↑, 1,  

Clinical Biomarkers ⓘ

EZH2↓, 1,   IL6↓, 1,   TP53↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoPv↑, 1,  
Total Targets: 79

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   MDA↓, 1,   ROS↓, 2,   SOD↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 2,  

Functional Outcomes ⓘ

cognitive↑, 1,   memory↑, 1,  
Total Targets: 8

Scientific Paper Hit Count for: miR-27a-3p, miR-27a-3p
4 Curcumin
1 Boswellia (frankincense)
1 Chemotherapy
1 Resveratrol
1 Quercetin
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

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