miR-34a Cancer Research Results

miR-34a, mir-34 precursor family: Click to Expand ⟱
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MiR-34a expression levels were correlated with tumor differentiation, lymphatic metastasis, clinical stages, and survival rates.

miR-34a is a well-known molecule transcriptionally induced by p53.

-Low miR-34a expression is common in cancers and is often associated with poor prognosis in various cancers, including breast, lung, colorectal, prostate, pancreatic, ovarian, and glioblastoma.
-High miR-34a expression is often associated with better prognosis and improved overall survival in various cancers.
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↓,

126- CUR,    Modulation of miR-34a in curcumin-induced antiproliferation of prostate cancer cells
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, PC3 - in-vitro, Pca, DU145
miR-34a↑, curcumin significantly upregulated the expression of miR‐34a, along with the downregulated expression of β‐catenin and c‐myc in three prostate cancer cell lines.
β-catenin/ZEB1↓, curcumin‐induced miR‐34a suppressed the activation of β‐catenin/c‐myc axis and inhibited cell proliferation of prostate cancer cells.
cMyc↓,
P21↑,
cycD1/CCND1↓,
PCNA↓,
TumCG↓, Curcumin inhibited cell growth of prostate cancer cells

405- CUR,  5-FU,    Curcumin activates a ROS/KEAP1/NRF2/miR-34a/b/c cascade to suppress colorectal cancer metastasis
- vitro+vivo, CRC, HCT116
Apoptosis↑, more pronounced increase in apoptosis in p53-deficient when compared to p53-proficient cells
TumCMig↓,
NRF2↑,
ROS↑, antioxidant N-acetylcysteine suppressed the induction of apoptosis by curcumin
MET↑, Curcumin induces MET and inhibits lung-metastases formation via inducing miR-34a
miR-34a↑, Notably, curcumin induced miR-34a and miR-34b/c expression in a ROS/NRF2-dependent and p53-independent manner.

456- CUR,    Curcumin Promoted miR-34a Expression and Suppressed Proliferation of Gastric Cancer Cells
- vitro+vivo, GC, SGC-7901
miR-34a↑,
TumCP↓,
TumCMig↓,
TumCI↓,
TumCCA↑, inhibited cell cycle progression in G0/G1-S phase
Bcl-2↓,
CDK4/6↓, CDK4
cycD1/CCND1↓,

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↓,

679- EGCG,  5-FU,    Epigallocatechin-3-gallate targets cancer stem-like cells and enhances 5-fluorouracil chemosensitivity in colorectal cancer
- in-vitro, CRC, NA
NOTCH1↓, Furthermore, EGCG suppressed Notch1
BMI1↓,
SUZ12↓,
EZH2↓,
miR-34a↑,
miR-200c↑,
miR-145↑,
CSCs↓, (EGCG), an active catechin present in green tea, has been shown to suppress CSC growth in various cancers

1654- FA,    Molecular mechanism of ferulic acid and its derivatives in tumor progression
- Review, Var, NA
AntiCan↑, FA has anti-inflammatory, analgesic, anti-radiation, and immune-enhancing effects and also shows anticancer activity,
Inflam↓,
RadioS↑,
ROS↑, FA can cause mitochondrial apoptosis by inducing the generation of intracellular reactive oxygen species (ROS)
Apoptosis↑,
TumCCA↑, G0/G1 phase
TumCMig↑, inducing autophagy; inhibiting cell migration, invasion, and angiogenesis
TumCI↓,
angioG↓,
ChemoSen↑, synergistically improving the efficacy of chemotherapy drugs and reducing adverse reactions.
ChemoSideEff↓,
P53↑, FA could increase the expression level of p53 in MIA PaCa-2 pancreatic cancer cells
cycD1/CCND1↓, while reducing the expression levels of cyclin D1 and cyclin-dependent kinase (CDK) 4/6.
CDK4↓,
CDK6↓,
TumW↓, FA treatment was found to reduce tumor weight in a dose-dependent manner, increase miR-34a expression, downregulate Bcl-2 protein expression, and upregulate caspase-3 protein expression
miR-34a↑,
Bcl-2↓,
Casp3↑,
BAX↑,
β-catenin/ZEB1↓, isoferulic acid dose-dependently downregulated the expression of β-catenin and MYC proto-oncogene (c-Myc), inducing apoptosis
cMyc↓,
Bax:Bcl2↑, FXS-3 can inhibit the activity of A549 cells by upregulating the Bax/Bcl-2 ratio
SOD↓, After treatment with FA, Cao et al. [40] observed an increase in ROS production and a decrease in superoxide dismutase activity and glutathione content in EC-1 and TE-4 oesophageal cancer cells
GSH↓,
LDH↓, FA could promote the release of lactate dehydrogenase (LDH)
ERK↑, A can activate the ERK1/2 pathway
eff↑, conjugated zinc oxide nanoparticles with FA (ZnONPs-FA) to act on hepatoma Huh-7 and HepG2 cells. The results showed that ZnONPs-FA could induce oxidative DNA damage and apoptosis by inducing ROS production.
JAK2↓, by inhibiting the JAK2/STAT6 immune signaling pathway
STAT6↓,
NF-kB↓, thus inhibiting the activation of NF-κB
PYCR1↓, FA can target PYCR1 and inhibit its enzyme activity in a concentration-dependent manner.
PI3K↓, FA inhibits the activation of the PI3K/AKT pathway
Akt↓,
mTOR↓, FA could significantly reduce the expression level of mTOR mRNA and Ki-67 protein in A549 lung cancer graft tissue
Ki-67↓,
VEGF↓,
FGFR1↓, FA is a novel FGFR1 inhibitor
EMT↓, FA can inhibit EMT
CAIX↓, selectively inhibit CAIX
LC3II↑, Autophagy vacuoles and increased LC3-II and p62 autophagy proteins were observed after treatment with this compound
p62↑,
PKM2↓, FA could inhibit the expression of PKM2 and block aerobic glycolysis
Glycolysis↓,
*BioAv↓, FA has poor solubility in water and a poor ability to pass through biological barriers [118]; therefore, the extent to which it is metabolized in vivo after oral administration is largely unknown

997- GA,    The Inhibitory Mechanisms of Tumor PD-L1 Expression by Natural Bioactive Gallic Acid in Non-Small-Cell Lung Cancer (NSCLC) Cells
- in-vitro, Lung, A549 - in-vitro, Lung, H292 - in-vitro, Nor, HUVECs
PD-L1↓, GA strongly decreases the expression levels of PD-L1 protein in A549 and H292 NSCLC cells
p‑EGFR↓,
p‑PI3K↓,
p‑Akt↓,
P53↑, GA upregulates the expression levels of p53 protein in a concentration-dependent manner
miR-34a↑, p53 indirectly regulates the expression levels of PD-L1 through inducing miR-34a in cancer cells
*toxicity↓, 400 μM GA inducing around 8% cell death which indicated that this concentration does not make much toxicity in normal cells

222- MFrot,  MF,    LF-MF inhibits iron metabolism and suppresses lung cancer through activation of P53-miR-34a-E2F1/E2F3 pathway
- in-vitro, Lung, A549
TumCG↓,
OS↑,
miR-34a↑, enhanced miR-34a transcription
E2Fs↓, E2F1/E2F3
P53↑,
TfR1/CD71↓, TfR1 protein levels
Ferritin↓, inhibits iron metabolism

2084- TQ,    Thymoquinone, as an anticancer molecule: from basic research to clinical investigation
- Review, Var, NA
*ROS↓, An interesting study reported that thymoquinone is actually a potent apoptosis inducer in cancer cells, but it exerts antiapoptotic effect through attenuating oxidative stress in other types of cell injury
*chemoPv↑, antioxidant activity of thymoquinone is responsible for its chemopreventive activities
ROS↑, other studies reported thymoquinone induce apoptosis in cancer cells by exerting oxidative damage
ROS⇅, Another hypothesis states that thymoquinone acts as an antioxidant at lower concentrations and a prooxidant at higher concentrations
MUC4↓, Torres et al. [17] revealed that thymoquinone down-regulates glycoprotein mucin 4 (MUC4)
selectivity↑, thymoquinone was found to inhibit DNA synthesis, proliferation, and viability of cancerous cells, such as LNCaP, C4-B, DU145, and PC-3, but not noncancerous BPH-1 prostate epithelial cells [20].
AR↓, Down-regulation of androgen receptor (AR) and cell proliferation regulator E2F-1 was indicated as the mechanism behind thymoquinone’s action in prostate cancer
cycD1/CCND1↓, expression of STAT3-regulated gene products, such as cyclin D1, Bcl-2, Bcl-xL, survivin, Mcl-1 and vascular endothelial growth factor (VEGF), was inhibited by thymoquinone, which ultimately increased apoptosis and killed cancer cells
Bcl-2↓,
Bcl-xL↓,
survivin↓,
Mcl-1↓,
VEGF↓,
cl‑PARP↑, induction of the cleavage of poly-(ADP-ribose) polymerase (PARP
ROS↑, In ALL cell line CEM-ss, thymoquinone treatment generated reactive oxygen species (ROS) and HSP70
HSP70/HSPA5↑,
P53↑, thymoquinone can induce apoptosis in MCF-7 breast cancer cells via the up-regulation of p53 expression
miR-34a↑, Thymoquinone significantly increased the expression of miR-34a via p53, and down-regulated Rac1 expression
Rac1↓,
TumCCA↑, In hepatic carcinoma, thymoquinone induced cell cycle arrest and apoptosis by repressing the Notch signaling pathway
NOTCH↓,
NF-kB↓, Evidence revealed that thymoquinone suppresses tumor necrosis factor (TNF-α)-induced NF-kappa B (NF-κB) activation
IκB↓, consequently inhibits the activation of I kappa B alpha (I-κBα) kinase, I-κBα phosphorylation, I-κBα degradation, p65 phosphorylation
p‑p65↓,
IAP1↓, down-regulated the expression of NF-κB -regulated antiapoptotic gene products, like IAP1, IAP2, XIAP Bcl-2, Bcl-xL;
IAP2↑,
XIAP↓,
TNF-α↓, It also inhibited monocyte chemo-attractant protein-1 (MCP-1), TNF-α, interleukin (IL)-1β and COX-2, ultimately reducing the NF-κB activation in pancreatic ductal adenocarcinoma cells
COX2↓,
Inflam↓, indicating its role as an inhibitor of proinflammatory pathways
α-tubulin↓, Without affecting the tubulin levels in normal human fibroblast, thymoquinone induces degradation of α and β tubulin proteins in human astrocytoma U87 cells and in T lymphoblastic leukaemia Jurkat cells, and thus exerts anticancer activity
Twist↓, thymoquinone treatment inhibits TWIST1 promoter activity and decreases its expression in breast cancer cell lines; leading to the inhibition of epithelial-mesenchymal transition (EMT)
EMT↓,
mTOR↓, thymoquinone also attenuated mTOR activity, and inhibited PI3K/Akt signaling in bladder cancer
PI3K↓,
Akt↓,
BioAv↓, Thymoquinone is chemically hydrophobic, which causes its poor solubility, and thus bioavailability. bioavailability of thymoquinone was reported ~58% with a lag time of ~23 min
ChemoSen↑, Some studies revealed that thymoquinone in combination with other chemotherapeutic drugs can show better anticancer activities
BioAv↑, Thymoquinone-loaded liposomes (TQ-LP) and thymoquinone loaded in liposomes modified with Triton X-100 (XLP) with diameters of about 100 nm were found to maintain stability, improve bioavailability and maintain thymoquinone’s anticancer activity
PTEN↑, Thymoquinone also induces apoptosis by up-regulating PTEN
chemoPv↑, A recent study showed that thymoquinone can potentiate the chemopreventive effect of vitamin D during the initiation phase of colon cancer in rat model
RadioS↑, thymoquinone also mediates radiosensitization and cancer chemo-radiotherapy
*Half-Life↝, Thymoquinone-loaded nanostructured lipid carrier (TQ-NLC) has been developed to improve its bioavailability (elimination half-life ~5 hours)
*BioAv↝, calculated absolute bioavailability of thymoquinone was reported ~58% with a lag time of ~23 min by Alkharfy et al.


Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   NRF2↑, 1,   PYCR1↓, 1,   ROS↑, 4,   ROS⇅, 1,   SOD↓, 1,  

Metal & Cofactor Biology ⓘ

Ferritin↓, 1,   TfR1/CD71↓, 1,  

Mitochondria & Bioenergetics ⓘ

FGFR1↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

CAIX↓, 1,   cMyc↓, 3,   Glycolysis↓, 1,   LDH↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 1,   Apoptosis↑, 3,   BAX↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 4,   Bcl-xL↓, 1,   Casp3↑, 1,   IAP1↓, 1,   IAP2↑, 1,   Mcl-1↓, 1,   miR-497↑, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   miR-145↑, 2,   miR-21↓, 2,   miR-27a-3p↓, 4,   miR-409-3p↑, 1,  

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   p62↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 4,   cl‑PARP↑, 1,   PARP1↓, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 2,   cycD1/CCND1↓, 5,   E2Fs↓, 1,   P21↑, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

BMI1↓, 1,   CSCs↓, 1,   EMT↓, 2,   ERK↑, 1,   miR-101↑, 1,   miR-34a↑, 12,   miR-429↑, 1,   mTOR↓, 2,   NOTCH↓, 1,   NOTCH1↓, 1,   PI3K↓, 2,   p‑PI3K↓, 1,   PTEN↑, 1,   STAT6↓, 1,   SUZ12↓, 1,   TumCG↓, 3,  

Migration ⓘ

CDK4/6↓, 1,   Ki-67↓, 1,   MET↑, 1,   miR-130a↓, 1,   miR-141↑, 1,   miR-155↓, 1,   miR-20↓, 1,   miR-200b↑, 1,   miR-200c↑, 2,   miR-206↑, 1,   miR-221↓, 1,   miR-491↑, 1,   miR‐222↓, 1,   MUC4↓, 1,   Rac1↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCMig↑, 1,   TumCP↓, 1,   Twist↓, 1,   α-tubulin↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

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

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 2,   IκB↓, 1,   JAK2↓, 1,   NF-kB↓, 2,   p‑p65↓, 1,   PD-L1↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CDK6↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 3,   eff↑, 1,   RadioS↑, 2,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   p‑EGFR↓, 1,   EZH2↓, 1,   Ferritin↓, 1,   Ki-67↓, 1,   LDH↓, 1,   PD-L1↓, 1,   SUZ12↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   chemoPv↑, 2,   ChemoSideEff↓, 1,   OS↑, 1,   TumW↓, 1,  
Total Targets: 118

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↝, 1,   Half-Life↝, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,   toxicity↓, 1,  
Total Targets: 8

Scientific Paper Hit Count for: miR-34a, mir-34 precursor family
6 Curcumin
2 5-fluorouracil
1 Boswellia (frankincense)
1 Chemotherapy
1 EGCG (Epigallocatechin Gallate)
1 Ferulic acid
1 Gallic acid
1 Magnetic Field Rotating
1 Magnetic Fields
1 Thymoquinone
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#:450  State#:%  Dir#:2
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