TumAuto Cancer Research Results

TumAuto, Tumor autophagy: Click to Expand ⟱
Source: HalifaxProj(activate)
Type:
Autophagy genes, including Atg3, Atg5, Atg6, Atg7, Atg10, Atg12, and Atg17.
Tumor autophagy refers to the process by which cancer cells degrade and recycle cellular components through autophagy, a cellular mechanism that helps maintain homeostasis and respond to stress. Autophagy can have dual roles in cancer, acting as both a tumor suppressor and a promoter, depending on the context.
Authophagy is the process used by cancer cells to “self-eat” to survive. Authophagy can be both good and bad. If authophagy is prolonged this will become a lethal process to cancer. On the other hand, for a short while (e.g. during chemotheraphy, radiotheraphy, etc.) authophagy is used by cancer cells to survive.
For example, Chloroquine is a blocker of autophagy and has been used in a lab setting to dramatically enhance tumor response to radiotherapy, chemotherapy.
Scientific Papers found: Click to Expand⟱
5430- AG,    Review of the pharmacological effects of astragaloside IV and its autophagic mechanism in association with inflammation
- Review, Stroke, NA
*cardioP↑, Review of the pharmacological effects of astragaloside IV and its autophagic mechanism in association with inflammation - PMC
*MitoP↑, The mechanism included promotion of mitophagy, which reduced generation of mitochondrial ROS and accumulation of damaged mitochondria[31].
*ROS↓, AS-IV can reduce ROS-mediated autophagosome accumulation and myocardial injury caused by I/R[21]
*mtDam↓,
*neuroP↓, Ischemic stroke MCAO in SD rats; OGD/R in HT22 cells A neuroprotective role (-) apoptosis (+) autophagy
TumAuto↓, For NSCLC cells treated with cisplatin, AS-IV inhibited the increased autophagy of proteins Beclin1 and LC3 I/II
*AntiDiabetic↑, Protective effect of AS-IV on diabetes

280- ALA,    Alpha‐lipoic acid inhibits lung cancer growth via mTOR‐mediated autophagy inhibition
- in-vivo, Lung, A549
p‑mTOR↑, significantly increased mTOR phosphorylation level by 76.9%
TumCG↓, LA suppressed lung cancer growth in mice.
TumAuto↓, (note this research paper takes the approach of wanting to reduce autophagy)
p‑P70S6K↑, phosphorylation level of p70S6K, a downstream target of mTOR, was increased by 83.2% when compared with controls

872- CUR,  RES,    New Insights into Curcumin- and Resveratrol-Mediated Anti-Cancer Effects
- in-vitro, BC, TUBO - in-vitro, BC, SALTO
TumCP↓,
tumCV↓,
p62↓, reduced by Cur
p62↑, accumulated by Res
TumAuto↑, Cur only
TumAuto↓, Res only
ROS↑, increased ROS with Res
ROS↓, decreased ROS with Cur or combination
CHOP↑, strongly upregulated by the curcumin/resveratrol combination

5069- dietSTF,    The Role of Intermittent Fasting in the Activation of Autophagy Processes in the Context of Cancer Diseases
- Review, Var, NA
Risk↓, IF has shown potential for reducing cancer risk and enhancing therapeutic efficacy by sensitizing tumor cells to chemotherapy and radiotherapy.
ChemoSen↑, intermittent fasting (IF) may enhance the effectiveness of chemotherapy and targeted therapies by activating autophagy. IF enhances the effectiveness of chemotherapy, including drugs such as cisplatin, cyclophosphamide, and doxorubicin
RadioS↑, disease stabilization, improved response to radiotherapy patients with glioma
*Dose↝, 16:8—16 h of fasting with an 8 h eating window;
*Dose↝, 5:2—consuming a standard number of calories for 5 days and reducing intake to 25% of daily requirements for 2 days;
*Dose↝, Eat–Stop–Eat—complete fasting for 24–48 h.
*LDL↓, IF during Ramadan (approximately 18 h of fasting for 29–30 days) reduces LDL cholesterol levels and increases HDL cholesterol in women, as well as reducing inflammatory markers such as CRP and TNF-α
*CRP↓,
*TNF-α↓,
TumAuto↓, Intermittent fasting activates autophagy as an adaptive mechanism to nutrient deprivation, which may modulate tumor development and treatment
GLUT1↓, fasting reduces the expression of glucose transporters GLUT1/2, which slow down cancer metabolism and increase the susceptibility of cancer cells to oxidative stress
GLUT2↓,
glucose↓, studies on cell and animal models have shown that intermittent fasting reduces glucose and insulin-like growth factor (IGF-1) levels [103], as well as insulin [104,105], resulting in the inhibition of the mTOR kinase pathway (PI3K/Akt/mTOR), suppress
IGF-1↓,
Insulin↓,
mTOR↓,
mTORC1↓, suppression of mTORC1 [22], and activation of AMPK through increased ADP/ATP ratio in cells, which supports autophagy and induces apoptosis
AMPK↑,
Warburg↓, Moreover, IF counteracts the Warburg effect by promoting oxidative phosphorylation, leading to an increase in the production of reactive oxygen species (ROS) and enhanced oxidative stress in cancer cells [106,108], causing DNA damage and the activati
OXPHOS↑,
ROS↑,
DNAdam↑,
JAK1↓, fasting reduces the production of adenosine by cancer cells, inhibiting the activation of the JAK1/STAT pathway, thereby reducing cancer cell proliferation
STAT↓,
TumCP↓,
QoL↑, reduction in IGF-1 levels, improved quality of life patients with multiple cancer types

975- Est,    Estrogen inhibits autophagy and promotes growth of endometrial cancer by promoting glutamine metabolism
- vitro+vivo, UEC, NA
GLS↑, in estrogen-sensitive UEC cell (UECC) (an ER inhibitor antagonist) could reverse these effects.
cMyc↑, three MYC subtypes (c-MYC, n-MYC and l-MYC) were increased after estrogen treatment
GlutMet↑,
tumCV↑,
TumAuto↓,

1441- HCQ,  Chemo,    Case report: stage 4 pancreatic cancer to remission using paricalcitol and hydroxychloroquine in addition to traditional chemotherapy
- Case Report, GBM, NA
TumAuto↓, Hydroxychloroquine has been shown to inhibit autophagy. Autophagy is a process of self-cannibalization in which injured cancer cells ingest pieces of themselves, such as organelles and macromolecules, to conserve energy, and, therefore, thrive.
Remission↑, have now enjoyed a complete response with my latest CA19-9 of just 15 U/mL and no evidence of active disease on my most recent CT scan.

1439- HCQ,    Acidic extracellular pH neutralizes the autophagy-inhibiting activity of chloroquine
- in-vitro, Melanoma, NA - in-vitro, CRC, HCT116
TumAuto↓, Inhibition of autophagy by administration of chloroquine (CQ) in combination anticancer therapies is currently evaluated in clinical trials.
eff↓, targeting autophagy in the tumor environment by CQ may be limited to well-perfused regions but not achieved in acidic regions, predicting possible limitations in efficacy of CQ in antitumor therapies.
other↓, CQ concentrations in the whole-cell lysate were 7-fold lower at pH 6.8 as compared with pH 7.4

5124- Sal,    Inhibition of the autophagic flux by salinomycin in breast cancer stem-like/progenitor cells interferes with their maintenance
- in-vitro, BC, NA
CSCs↓, Salinomycin (Sal), a K+/H+ ionophore, has recently been shown to be at least 100 times more effective than paclitaxel in reducing the proportion of breast CSCs
LC3II↑, Sal-induced accumulation of LC3-II
other↓, Sal inhibits autophagy flux
lysosome↓, Sal treatment inhibits lysosomal activity
CTSZ↓, The combined activity of cathepsins Z, B, L, and S was significantly lower in Sal–treated cells, as were the specific activities of CTSB and CTSL, indicating that Sal significantly inhibits the activity of cathepsins
CTSB↓,
CTSL↓,
CTSS↓,
autoF↓, Inhibition of the autophagic flux by salinomycin
TumAuto↓, In this study, we reported the inhibitory effect of Sal on autophagy and its consequence on the crosstalk with the apoptosis pathway.

5110- SSE,    Autophagy inhibition through PI3K/Akt increases apoptosis by sodium selenite in NB4 cells
- in-vitro, AML, APL NB4
Apoptosis↑, Selenium possesses the chemotherapeutic feature by inducing apoptosis in cancer cell with trivial side effects on normal cells.
selectivity↑,
TumAuto↓, role of autophagy in selenium-induced apoptosis in NB4 cells.
PI3K↓, while the PI3K/Akt signaling pathway is down- regulated.
Akt↓,


Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

OXPHOS↑, 1,   ROS↓, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

Insulin↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   cMyc↑, 1,   GLS↑, 1,   glucose↓, 1,   GLUT2↓, 1,   GlutMet↑, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 1,  

Transcription & Epigenetics ⓘ

other↓, 2,   tumCV↓, 1,   tumCV↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,  

Autophagy & Lysosomes ⓘ

autoF↓, 1,   LC3II↑, 1,   lysosome↓, 1,   p62↓, 1,   p62↑, 1,   TumAuto↓, 9,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   CTSB↓, 1,   CTSL↓, 1,   CTSS↓, 1,   IGF-1↓, 1,   mTOR↓, 1,   p‑mTOR↑, 1,   mTORC1↓, 1,   p‑P70S6K↑, 1,   PI3K↓, 1,   STAT↓, 1,   TumCG↓, 1,  

Migration ⓘ

TumCP↓, 2,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

CTSZ↓, 1,   JAK1↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↓, 1,   RadioS↑, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

QoL↑, 1,   Remission↑, 1,   Risk↓, 1,  
Total Targets: 48

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS↓, 1,  

Mitochondria & Bioenergetics ⓘ

mtDam↓, 1,  

Core Metabolism/Glycolysis ⓘ

LDL↓, 1,  

Autophagy & Lysosomes ⓘ

MitoP↑, 1,  

Immune & Inflammatory Signaling ⓘ

CRP↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 3,  

Clinical Biomarkers ⓘ

CRP↓, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   cardioP↑, 1,   neuroP↓, 1,  
Total Targets: 11

Scientific Paper Hit Count for: TumAuto, Tumor autophagy
2 hydroxychloroquine
1 Astragalus
1 Alpha-Lipoic-Acid
1 Curcumin
1 Resveratrol
1 diet Short Term Fasting
1 Estrogen
1 Chemotherapy
1 salinomycin
1 Selenite (Sodium)
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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