miR-200b Cancer Research Results

miR-200b, miR-200b: Click to Expand ⟱
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MicroRNA-200b (miR-200b) is encoded by the MIR200B gene, which is part of the microRNA-200 family located on chromosome 1 in humans. This microRNA plays a crucial role in the regulation of gene expression, particularly in processes related to epithelial-to-mesenchymal transition (EMT), cell proliferation, differentiation, and apoptosis.

miR-200b is generally considered antitumorigenic in many contexts. It plays a critical role in maintaining epithelial characteristics and inhibiting EMT, which is associated with reduced metastatic potential. By targeting genes involved in cell migration and invasion, miR-200b can suppress tumor progression.
Scientific Papers found: Click to Expand⟱
4812- ASTX,    Astaxanthin suppresses the metastasis of colon cancer by inhibiting the MYC-mediated downregulation of microRNA-29a-3p and microRNA-200a
- in-vitro, CRC, HCT116
miR-29b↑, AXT increases miR-29a-3p and miR-200a expression, and thereby suppresses the expression of MMP2 and ZEB1, respectively.
miR-200b↑,
MMP2↓, Astaxanthin suppresses MMP2 activity through upregulation of miR-29a-3p
Zeb1↓,
EMT↓, As a result, AXT represses the epithelial-mesenchymal transition (EMT) of CRC cells.
Apoptosis↑, AXT suppresses oral carcinomas by inducing apoptosis through the inhibition of Erk/MAPK and PI3K/Akt signaling
ERK↓,
MAPK↓,
PI3K↓,
Akt↓,
MMPs↓, AXT reduces the metastasis of cancer cells by decreasing the expression of MMPs,
TumMeta↓, Astaxanthin suppresses the metastatic activity of colon cancer cell in in vivo model

2767- Bos,    The potential role of boswellic acids in cancer prevention and treatment
- Review, Var, NA
*Inflam↓, profound application as a traditional remedy for various ailments, especially inflammatory diseases including asthma, arthritis, cerebral edema, chronic pain syndrome, chronic bowel diseases, cancer
AntiCan↑,
*MAPK↑, 11-keto-BAs can stimulate Mitogen-activated protein kinases (MAPK) and mobilize the intracellular Ca(2+) that are important for the activation of human polymorphonuclear leucocytes (PMNL)
*Ca+2↝,
p‑ERK↓, AKBA prohibited the phosphorylation of extracellular signal-regulated kinase-1 and -2 (Erk-1/2) and impaired the motility of meningioma cells stimulated with platelet-derived growth factor BB
TumCI↓,
cycD1/CCND1↓, In the case of colon cancer, BA treatment on HCT-116 cells led to a decrease in cyclin D, cyclin E, and Cyclin-dependent kinases such as CDK2 and CDK4, along with significant reduction in phosphorylated Rb (pRb)
cycE/CCNE↓,
CDK2↓,
CDK4↓,
p‑RB1↓,
*NF-kB↓, convey inhibition of NF-kappaB and subsequent down-regulation of TNF-alpha expression in activated human monocytes
*TNF-α↓,
NF-kB↓, PC-3 prostate cancer cells in vitro and in vivo by inhibiting constitutively activated NF-kappaB signaling by intercepting the activity of IkappaB kinase (IKK
IKKα↓,
MCP1↓, LPS-challenged ApoE-/- mice via inhibition of NF-κB and down regulation of MCP-1, MCP-3, IL-1alpha, MIP-2, VEGF, and TF
IL1α↓,
MIP2↓,
VEGF↓,
Tf↓,
COX2↓, pancreatic cancer cell lines, AKBA inhibited the constitutive expression of NF-kB and caused suppression of NF-kB regulated genes such as COX-2, MMP-9, CXCR4, and VEGF
MMP9↓,
CXCR4↓,
VEGF↓,
eff↑, AKBA and aspirin revealed that AKBA has higher potential via modulation of the Wnt/β-catenin pathway, and NF-kB/COX-2 pathway in adenomatous polyps
PPARα↓, AKBA is also responsible for down-regulation of PPAR-alpha and C/EBP-alpha in a dose and temporal dependent manner in mature adipocytes, ultimately leading to pparlipolysis
lipid-P?,
STAT3↓, activation of STAT-3 in human MM cells could be inhibited by AKBA
TOP1↓, (PKBA; a semisynthetic analogue of 11-keto-β-boswellic acid), had been reported to influence the activity of topoisomerase I & II,
TOP2↑,
5HT↓, (5-LO), responsible for catalyzing the synthesis of leukotrienes from arachidonic acid and human leucocyte elastase (HLE), and serine proteases involved in several inflammatory processes, is considered to be a potent molecular target of BA derivative
p‑PDGFR-BB↓, BA up-regulates SHP-1 with subsequent dephosphorylation of PDGFR-β and downregulation of PDGF-dependent signaling after PDGF stimulation, thereby exerting an anti-proliferative effect on HSCs hepatic stellate cells
PDGF↓,
AR↓, AKBA targets different receptors that include androgen receptor (AR), death receptor 5 (DR5), and vascular endothelial growth factor receptor 2 (VEGFR2), and leads to the inhibition of proliferation of prostate cancer cells
DR5↑, induced expression of DR4 and DR5.
angioG↓, via apoptosis induction and suppression of angiogenesis
DR4↑,
Casp3↑, AKBA resulted in activation of caspase-3 and caspase-8, and initiation of poly (ADP) ribose polymerase (PARP) cleavage.
Casp8↑,
cl‑PARP↑,
eff↑, AKBA was preincubated with LY294002 or wortmannin (inhibitors of PI3K), it caused a significant enhancement of apoptosis in HT-29 cells
chemoPv↑, chemopreventive response of AKBA was estimated against intestinal adenomatous polyposis through the inhibition of the Wnt/β-catenin and NF-κB/cyclooxygenase-2 signaling pathway
Wnt↓,
β-catenin/ZEB1↓,
ascitic↓, AKBA by the suppression of ascites,
Let-7↑, AKBA could up-regulate the expression of let-7 and miR-200
miR-200b↑,
eff↑, anti-tumorigenic effects of curcumin and AKBA on the regulation of specific cancer-related miRNAs in colorectal cancer cells, and confirmed their protective action
MMP1↓, . It can inhibit the expression of MMP-1, MMP-2, and MMP-9 mRNAs along with secretions of TNF-α and IL-1β in THP-1 cells.
MMP2↓,
eff↑, combined administration of metformin, an anti-diabetic drug, and boswellic acid nanoparticles exhibited significant synergism through the inhibition of MiaPaCa-2 pancreatic cancer cell proliferation
BioAv↓, BA as a therapeutic drug is its poor bioavailability
BioAv↑, administration of BSE-018 concomitantly with a high-fat meal led to several-fold increased areas under the plasma concentration-time curves as well as peak concentrations of beta-boswellic acid (betaBA)
Half-Life↓, drug needs to be given orally at the interval of six hours due to its calculated half- life, which was around 6 hrs.
toxicity↓, BSE has been found to be a safe drug without any adverse side reactions, and is well tolerated on oral administration.
Dose↑, Boswellia serrata extract to the maximum amount of 4200 mg/day is not toxic and it is safe to use though it shows poor bioavailability
BioAv↑, Approaches like lecithin delivery form (Phytosome®), nanoparticle delivery systems like liposomes, emulsions, solid lipid nanoparticles, nanostructured lipid carriers, micelles and poly (lactic-co-glycolic acid) nanoparticles
ChemoSen↑, Like any other natural products BA can also be effective as chemosensitizer

1422- Bos,    Boswellic acid exerts antitumor effects in colorectal cancer cells by modulating expression of the let-7 and miR-200 microRNA family
- in-vitro, CRC, NA - in-vivo, NA, NA
5LO↓, boswellic acids, is known to be a non-redox and non-competitive inhibitor of 5-lipoxygenase
TumCG↓,
Let-7↑,
miR-200b↑, AKBA significantly up-regulated expression of the let-7 and miR-200 families in various CRC cell lines
NF-kB↓,
cMyc↓,
cycD1/CCND1↓,
MMP9↓,
CXCR4↓,
VEGF↓,
Bcl-xL↓,
survivin↓,
IAP1↓,
XIAP↓,
TumCG↓,
CDK6↓,
Vim↓,
E-cadherin↑,

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↓,

818- GAR,  GB,    Garcinol Sensitizes NSCLC Cells to Standard Therapies by Regulating EMT-Modulating miRNAs
- in-vitro, Lung, A549
miR-205↑,
Let-7↑,
Apoptosis↑, Garcinol Potentiates Apoptosis Induction by Erlotinib
miR-200b↑,
miR-218↑,


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 ⓘ

lipid-P?, 1,  

Metal & Cofactor Biology ⓘ

Tf↓, 1,  

Mitochondria & Bioenergetics ⓘ

XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   PPARα↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   Bcl-xL↓, 1,   Casp3↑, 1,   Casp8↑, 1,   DR4↑, 1,   DR5↑, 1,   IAP1↓, 1,   MAPK↓, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

miR-205↑, 1,   miR-21↓, 1,   miR-218↑, 1,   miR-27a-3p↓, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   p‑RB1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   ERK↓, 1,   p‑ERK↓, 1,   Let-7↑, 3,   miR-34a↑, 1,   PI3K↓, 1,   STAT3↓, 1,   TOP1↓, 1,   TOP2↑, 1,   TumCG↓, 2,   Wnt↓, 1,  

Migration ⓘ

5LO↓, 1,   E-cadherin↑, 1,   miR-200b↑, 5,   miR-29b↑, 1,   MMP1↓, 1,   MMP2↓, 2,   MMP9↓, 2,   MMPs↓, 1,   PDGF↓, 1,   TumCI↓, 1,   TumMeta↓, 1,   Vim↓, 1,   Zeb1↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   p‑PDGFR-BB↓, 1,   VEGF↓, 3,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CXCR4↓, 2,   IKKα↓, 1,   IL1α↓, 1,   MCP1↓, 1,   MIP2↓, 1,   NF-kB↓, 2,  

Synaptic & Neurotransmission ⓘ

5HT↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   ChemoSen↑, 1,   Dose↑, 1,   eff↑, 4,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   ascitic↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   chemoPv↑, 2,   toxicity↓, 1,  
Total Targets: 74

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Cell Death ⓘ

MAPK↑, 1,  

Migration ⓘ

Ca+2↝, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 2,   NF-kB↓, 1,   TNF-α↓, 1,  
Total Targets: 6

Scientific Paper Hit Count for: miR-200b, miR-200b
2 Boswellia (frankincense)
1 Astaxanthin
1 Curcumin
1 Garcinol
1 gefitinib, erlotinib
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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