miR-19b Cancer Research Results

miR-19b, MicroRNA-19: Click to Expand ⟱
Source:
Type: oncogenic
Overexpression of miR-19 is strongly associated with cancer invasion and metastasis.
Scientific Papers found: Click to Expand⟱
429- CUR,    TAp63α Is Involved in Tobacco Smoke-Induced Lung Cancer EMT and the Anti-cancer Activity of Curcumin via miR-19 Transcriptional Suppression
- in-vitro, Lung, H1299 - in-vitro, Lung, A549
TAp63α↑,
E-cadherin↑,
ZO-1↑,
Vim↓,
N-cadherin↓,
miR-19b↓, miR-19a, miR-19b

7324- GSE,    A Pilot Study of a Grape Seed Procyanidin Extract for Lung Cancer Chemoprevention
- Trial, Lung, NA
BioAv↑, a standardized GSE complexed with soy phospholipids to enhance bio-availability, in heavy active and former smokers
toxicity↝, In general, three months of LP, reaching the highest dose per study protocol was well tolerated and no dosing adjustment was necessary.
Ki-67↓, significantly decreased bronchial Ki-67 LI by an average of 55%
miR-106b↓, with concomitant decreases in serum microRNA (miR) -19a, -19b and -106b
chemoPv↑, findings nonetheless support the continued clinical translation of GSE as an anti-neoplastic and chemopreventive agent against lung cancer.
Dose↝, 1 capsule (cap), 450 mg/cap/day for week one, 2 caps/day for week 2, 3 caps/day for week 3, then 4 cap/day for the rest of the treatment duration as tolerated.
miR-19b↓, Figure 5 downregulating oncomirs miR19-a, -19b, -106b a
PTEN↑, increases in tumor suppressors PTEN, IGF2R and decrease in activated p-Akt by miR-19a/b
IGF-2R↑,
p‑Akt↓,
PGE2↓, decreases in PGE2 and PGI2 due to COX-2 inhibition
PGI2↓,
COX2/PTGS2↓,
Apoptosis↑, GSE increases apoptosis, decreases cell proliferation, decreases inflammation,
TumCP↓,
Inflam↓,
cardioP↑, favorable side effect profiles that may also be cardio-protective,

7322- GSE,    MicroRNA-19a/b mediates grape seed procyanidin extract-induced anti-neoplastic effects against lung cancer
- vitro+vivo, Lung, A549 - in-vitro, Lung, H520 - in-vitro, Lung, H1299 - in-vitro, Nor, BEAS-2B
miR-19b↓, We found that GSE significantly down-regulated oncomirs miR-19a and −19b in a variety of lung neoplastic cells.
IGF-2R↑, GSE also increased mRNA and protein levels of insulin-like growth factor II receptor (IGF-2R) and phosphatase and tensin homolog (PTEN), both predicted targets of miR-19a and −19b.
PTEN↑,
p‑Akt↓, Furthermore, GSE significantly increased PTEN activity and decreased AKT phosphorylation in A549 cells.
Dose↝, All dosing regimen − 200, 300 and 400 mg/kg/day (containing GSE 56, 84, 112 mg/kg/day, respectively) for up to 8 weeks were well tolerated by nude mice.

4693- PTS,    Pterostilbene in the treatment of inflammatory and oncological diseases
BioAv↑, PTS is rapidly absorbed, contributing to its superior oral bioavailability of approximately 80%–95%
*Inflam↓, PTS exhibits anti-inflammatory, antioxidant, and antitumour properties, potentially making it a promising candidate for clinical applications
*antiOx↑,
AntiTum↑,
BBB↑, The ability of PTS to cross the blood-brain barrier efficiently not only broadens its therapeutic scope
Half-Life↝, The majority of Pterostilbene’s glucuronide-conjugated metabolites are excreted within 12 h post-administration, indicating rapid renal and total serum clearance
*ROS↓, PTS can reduce oxidative stress and counteract ROS like H2O2 and O2
*NRF2↑, PTS activates the phosphorylation of AMPK and AKT, prompting the shift of Nrf2 from the cytoplasm into the nucleus. This action then heightens the expression of Nrf2-regulated genes, NQO1 and HO-1
*NQO1↑,
*HO-1↑,
PTEN↑, PTS enhances PTEN expression in liver cancer cells by directly inhibiting miR-19a, which leads to reduced cell growth, cell cycle halt at the S phase, increased apoptosis, and decreased cell invasion
miR-19b↓,
TumCCA↑,
ER Stress↑, PTS administration can activate ERS and elevate levels of ERS-associated molecules like p-PERK, ATF4, and CHOP.
PERK↑,
ATF4↑,
CHOP/DDIT3↑,
Ca+2↝, facilitates the transfer of Ca2+ from the endoplasmic reticulum to the cytoplasm,
EMT↓, Pterostilbene inhibits epithelial-mesenchymal transition and apoptosis in tumors
NF-kB↓, downregulates NFκB, Twist1, and Vimentin and amplifies E-cadherin expression
Twist↓,
Vim↓,
E-cadherin↑,
ChemoSen↑, combined use of PTS and autophagy inhibitors has been shown to improve the therapeutic efficacy of chemotherapy drugs against both chemotherapy-sensitive and chemotherapy-resistant cancer cells.
toxicity∅, Remarkably, even at a high dose of 3,000 mg/(kg·d), no observable toxic side effects were detected in animal subjects
toxicity↝, some studies have raised concerns about potential liver toxicity at high doses

82- QC,  ATG,    Arctigenin in combination with quercetin synergistically enhances the anti-proliferative effect in prostate cancer cells
- in-vitro, Pca, LNCaP
AR↓,
PI3K/Akt↓, The combination treatment significantly inhibited both AR and PI3K/Akt pathways compared to control.
miR-21↓,
STAT3↓,
BAD↓,
PRAS40↓,
GSK‐3β↓,
PSA↓,
NKX3.1↑,
Bax:Bcl2↑, a significantly increased ratio of Bax to Bcl-2 protein expression was observed in LAPC-4 cells by the combination treatment compared to Q alone, and a trend to increase in LNCaP cells
miR-19b↓,
miR-148a↓,
AMPKα↓,
TumCP↓, The anti-proliferative activity of arctigenin was 10-20 fold stronger than quercetin in both cell lines.
chemoPv↑, combination of arctigenin and quercetin, that target similar pathways, at low physiological doses, provides a novel regimen with enhanced chemoprevention in prostate cancer.
TumCMig↓, Enhanced inhibition of cell migration


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:


NA, unassigned(tgid=0) ⓘ

IGF-2R↑, 2,   miR-106b↓, 1,   PGI2↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

PI3K/Akt↓, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↓, 2,   Apoptosis↑, 1,   BAD↓, 1,   Bax:Bcl2↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

AMPKα↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

miR-21↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   ER Stress↑, 1,   PERK↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

NKX3.1↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TAp63α↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

EMT↓, 1,   GSK‐3β↓, 1,   PTEN↑, 3,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↝, 1,   E-cadherin↑, 2,   Ki-67↓, 1,   miR-148a↓, 1,   miR-19b↓, 5,   N-cadherin↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   Twist↓, 1,   Vim↓, 2,   ZO-1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   PGE2↓, 1,   PSA↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   ChemoSen↑, 1,   Dose↝, 2,   Half-Life↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

AR↓, 1,   Ki-67↓, 1,   PSA↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiTum↑, 1,   cardioP↑, 1,   chemoPv↑, 2,   PRAS40↓, 1,   toxicity↝, 2,   toxicity∅, 1,  
Total Targets: 52

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   HO-1↑, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  
Total Targets: 6

Scientific Paper Hit Count for: miR-19b, MicroRNA-19
2 Grapeseed extract
1 Curcumin
1 Pterostilbene
1 Quercetin
1 Arctigenin
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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