α-tubulin Cancer Research Results

α-tubulin, α-tubulin: Click to Expand ⟱
Source:
Type:
α-Tubulin is a protein that is a component of microtubules, which are dynamic structures that play a crucial role in various cellular processes, including cell division, cell migration, and intracellular transport.
High α-tubulin expression is associated with poor prognosis, increased tumor size, and metastasis. α-Tubulin expression is also correlated with resistance to chemotherapy and hormone therapy. Generally, high α-tubulin expression is associated with:
      Poor prognosis
      Increased tumor size
      Metastasis
      Resistance to chemotherapy and radiation therapy
      Poor response to treatment

Low α-tubulin expression is associated with:
      Better prognosis
      Smaller tumor size
      Less metastasis
      Better response to chemotherapy and radiation therapy
      Better response to treatment
Scientific Papers found: Click to Expand⟱
2497- Fenb,    In vitro anti-tubulin effects of mebendazole and fenbendazole on canine glioma cells
- in-vitro, GBM, NA
Dose?, mean inhibitory concentration (IC50 ) ... fenbendazole were 0.550 ± 0.015, 1.530 ± 0.159 and 0.690 ± 0.095 μM
selectivity↑, treatment of primary canine fibroblasts for 72 h at IC50 showed no significant effect.
TumCD↑, Mebendazole and fenbendazole are cytotoxic in canine glioma cell lines in vitro and may be good candidates for treatment of canine gliomas.
α-tubulin↓, Immunofluorescence studies showed disruption of tubulin after treatment

2500- meben,    Antiparasitic mebendazole shows survival benefit in 2 preclinical models of glioblastoma multiforme
- in-vitro, GBM, U87MG - in-vivo, GBM, NA
α-tubulin↓, mechanism of action for MBZ and other benzimidazoles is to bind to the tubulin subunits in the gut epithelium of the parasite, preventing polymerization of the tubulin,
AntiCan↑, MBZ and ABZ have shown preclinical anticancer activity in adrenocortical carcinoma, lung cancer, ovarian cancer, and melanoma cells
TumCG↓, confirmed that the tumor growth was inhibited by MBZ treatment
OS↑, With the addition of MBZ to the treatment regimen, the mean survival was extended to 50 days
VEGF↓, Other mechanisms have been proposed for benzimidazole, such as inhibition of VEGF and HIF-1α e
Hif1a↓,

1664- PBG,    Anticancer Activity of Propolis and Its Compounds
- Review, Var, NA
Apoptosis↑,
TumCMig↓,
TumCCA↑,
TumCP↓,
angioG↓,
P21↑, upregulating p21 and p27 expression
p27↑,
CDK1↓, thanol-extracted Cameroonian propolis increased the amount of DU145 and PC3 cells in G0/G1 phase, down-regulated cell cycle proteins (CDK1, pCDK1, and their related cyclins A and B)
p‑CDK1↓,
cycA1/CCNA1↓,
CycB/CCNB1↓,
P70S6K↓, Caffeic acid phenylethyl ester has been shown to inhibit the S6 beta-1 ribosomal protein kinase (p70S6K),
CLDN2↓, inhibition of NF-κB may be involved in the decrease of claudin-2 mRNA level
HK2↓, Chinese poplar propolis has been shown to significantly reduce the level of glycolysis at the stage of action of hexokinase 2 (HK2), phosphofructokinase (PFK), muscle isozyme pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA)
PFK↓,
PKM2↓,
LDHA↓,
TLR4↓, hinese propolis, as well as CAPE, inhibits breast cancer cell proliferation in the inflammatory microenvironment by inhibiting the Toll-like receptor 4 (TLR4) signal pathway
H3↓, Brazilian red propolis bioactive isoflavonoid, down-regulates the alpha-tubulin, tubulin in microtubules, and histone H3 genes
α-tubulin↓,
ROS↑, CAPE also affects the apoptotic intrinsic pathway by increasing ROS production
Akt↓, CAPE induces apoptosis by decreasing the levels of proteins related to carcinogenesis, including Akt, GSK3b, FOXO1, FOXO3a, NF-kB, Skp2 and cyclin D1
GSK‐3β↓,
FOXO3↓,
NF-kB↓,
cycD1/CCND1↓,
MMP↓, It was found that chrysin caused a loss of mitochondria membrane potential (MMP) while increasing the production of reactive oxygen species (ROS), cytoplasmic Ca2+ levels, and lipid peroxidation
ROS↑,
i-Ca+2↑,
lipid-P↑,
ER Stress↑, Chrysin also induced endoplasmic reticulum (ER) stress by activating unfolded protein response proteins (UPR) such as PRKR-like ER kinase (PERK), eukaryotic translation initiation factor 2α (eIF2α), and 78 kDa glucose-regulated protein (GRP78)
UPR↑,
PERK↑,
eIF2α↑,
GRP78/BiP↑,
BAX↑, CAPE activated Bax protein
PUMA↑, CAPE also significantly increased PUMA expression
ROS↑, Northeast China causes cell apoptosis in human gastric cancer cells with increased production of reactive oxygen species (ROS) and reduced mitochondrial membrane potential.
MMP↓,
Cyt‑c↑, release of cytochrome C from mitochondria to the cytoplasm is observed, as well as the activation of cleaved caspases (8, 9, and 3) and PARP
cl‑Casp8↑,
cl‑Casp8↑,
cl‑Casp3↑,
cl‑PARP↑,
eff↑, administration of Iranian propolis extract in combination with 5-fluorouracil (5-FU) significantly reduced the number of azaxymethane-induced aberrant crypt foci compared to 5-FU or propolis alone.
eff↑, Propolis may also have a positive effect on the efficacy of photodynamic therapy (PDT). enhances the intracellular accumulation of protoporphyrin IX (PpIX) in human epidermoid carcinoma cells
RadioS↑, breast cancer patients undergoing radiotherapy and supplemented with propolis had a statistically significant longer median disease-free survival time than the control group
ChemoSen↑, confirmed that propolis mouthwash is effective and safe in the treatment of chemo- or radiotherapy-induced oral mucositis in cancer patients.
eff↑, Quercetin, ferulic acid, and CAPE may also influence the MDR of cancer cells by inhibiting P-gp expression

4955- PEITC,    Phenethyl isothiocyanate-induced cytoskeletal changes and cell death in lung cancer cells
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
TumCG↓, The observed growth-inhibitory effect of PEITC was dose-dependent, but time-dependence was observed only at higher concentrations.
α-tubulin↓, PEITC induced disassembly of actin stress fibers and degradation of tubulin which, most likely, contributed to the induction of cell death.
TumCD↑,
TumCCA↑, 24-h incubation caused G2/M cell cycle arrest, the fraction of G2/M cells decreased in a dose- and time-dependent manner in favor of cells with sub-G1 DNA content
Apoptosis↑, apoptosis-inducing potency of PEITC is probably the main factor responsible for cell growth inhibition.

3000- PL,    Biological and physical approaches on the role of piplartine (piperlongumine) in cancer
- in-vitro, Nor, HUVECs - in-vitro, Laryn, HEp2
Inflam↓, anti-inflammatory and antitumor activity.
AntiTum↑,
*α-tubulin↓, PL inhibits α-tubulin expression
selectivity↑, PL appeared to have no effect on the migration and invasion ability of normal or neoplastic cells
HIF2a↓, Other groups have expanded the knowledge of the biological properties of PL and suggested, inter alia, that PL inhibits hypoxia inducible factor-2 (HIF-2) transcription
MCP1↓, reduced the MCP-1 levels,

966- RT,    Antioxidant Mechanism of Rutin on Hypoxia-Induced Pulmonary Arterial Cell Proliferation
- vitro+vivo, Nor, NA
*ROS↓, (NAC), a scavenger of ROS, abolished or diminished the capability of rutin in repressing hypoxia-induced cell proliferation. ****
*NOX4↓, rutin decreased the up-regulation of Nox4 induced by hypoxia
*Hif1a↓, Upregulated Expression of HIF-1α Induced by Hypoxia Was Depressed by Rutin
*α-tubulin↓, Rutin reversed this increasing expression of α-tubulin, and the reversed effect was attenuated after scavenging ROS with NAC.

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 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 ⓘ

lipid-P↑, 1,   ROS↑, 5,   ROS⇅, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

HK2↓, 1,   LDHA↓, 1,   PFK↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   cl‑Casp3↑, 1,   cl‑Casp8↑, 2,   Cyt‑c↑, 1,   IAP1↓, 1,   IAP2↑, 1,   Mcl-1↓, 1,   p27↑, 1,   PUMA↑, 1,   survivin↓, 1,   TumCD↑, 2,  

Transcription & Epigenetics ⓘ

H3↓, 1,  

Protein Folding & ER Stress ⓘ

eIF2α↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   HSP70/HSPA5↑, 1,   PERK↑, 1,   UPR↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,   cl‑PARP↑, 2,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   p‑CDK1↓, 1,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 2,   P21↑, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   FOXO3↓, 1,   GSK‐3β↓, 1,   miR-34a↑, 1,   mTOR↓, 1,   NOTCH↓, 1,   P70S6K↓, 1,   PI3K↓, 1,   PTEN↑, 1,   TumCG↓, 2,  

Migration ⓘ

i-Ca+2↑, 1,   CLDN2↓, 1,   MUC4↓, 1,   Rac1↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   Twist↓, 1,   α-tubulin↓, 5,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,   HIF2a↓, 1,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 2,   IκB↓, 1,   MCP1↓, 1,   NF-kB↓, 2,   p‑p65↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

AR↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   chemoPv↑, 1,   OS↑, 1,  
Total Targets: 83

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

NOX4↓, 1,   ROS↓, 2,  

Migration ⓘ

α-tubulin↓, 2,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   Half-Life↝, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,  
Total Targets: 7

Scientific Paper Hit Count for: α-tubulin, α-tubulin
1 Fenbendazole
1 mebendazole
1 Propolis -bee glue
1 Phenethyl isothiocyanate
1 Piperlongumine
1 Rutin
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

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