Crocetin / Casp3 Cancer Research Results

Cro, Crocetin: Click to Expand ⟱
Features:
Crocetin is a carotenoid pigment found in saffron (Crocus sativus) and has been studied for its potential anti-cancer properties. Research has shown that crocetin may have anti-tumor and anti-proliferative effects, inhibiting the growth of various types of cancer cells.
Crocetin is a carotenoid dicarboxylic acid derived from saffron (Crocus sativus) and is a metabolite of crocin. It is lipophilic and more bioavailable than crocin. In cancer research, crocetin is studied mainly in preclinical models, where it appears to influence apoptosis, inflammation, angiogenesis, and redox signaling. It is not a primary cytotoxic chemotherapeutic, but a signaling and stress-modulating compound.
Mechanistic themes reported:
-NF-κB suppression
-PI3K/AKT pathway modulation
-MAPK signaling effects
-Apoptosis induction (mitochondrial pathway)
-Anti-angiogenic signaling (VEGF reduction)
-Redox modulation (context-dependent antioxidant / pro-oxidant behavior)

Evidence level: predominantly cell culture and animal models.
Reported to modulate glycolytic metabolism and lactate production (model-dependent); not established as a direct LDH enzymatic inhibitor

Crocetin (Cro) — Cancer-Oriented Time-Scale Flagged Pathway Table
Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 Intrinsic apoptosis (mitochondrial pathway) Bax ↑; Bcl-2 ↓; caspases ↑ (reported) ↔ (less activation) G Cell death signaling Apoptosis induction via mitochondrial membrane disruption is one of the most frequently reported tumor effects.
2 NF-κB inflammatory signaling NF-κB ↓; cytokines/COX-2 ↓ (reported) Inflammation tone ↓ R, G Anti-inflammatory modulation Reduction of inflammatory transcription may contribute to anti-proliferative and anti-invasive effects.
3 PI3K / AKT survival pathway AKT phosphorylation ↓ (reported; model-dependent) ↔ R, G Growth suppression Observed in several tumor cell systems; should be presented as context-dependent.
4 MAPK signaling (ERK / JNK / p38) Stress MAPK modulation (variable direction) ↔ P, R, G Signal reprogramming JNK activation and ERK suppression have been reported in some models; effects vary by cell type.
5 ROS / redox modulation ROS ↑ (pro-apoptotic) or ROS ↓ (antioxidant) depending on dose Oxidative stress ↓ (protective models) P, R, G Redox modulation (biphasic) Crocetin can behave as antioxidant in normal cells and pro-oxidant in tumor contexts at higher concentrations.
6 Cell-cycle arrest G0/G1 or G2/M arrest ↑ (reported) ↔ G Cytostasis Often secondary to survival pathway suppression and stress signaling.
7 Angiogenesis signaling (VEGF) VEGF ↓; angiogenic signaling ↓ (reported) ↔ G Anti-angiogenic support Observed in some in vitro and animal tumor models; typically secondary to NF-κB/AKT changes.
8 Metabolic reprogramming (glycolysis tone) Lactate ↓ (reported; indirect) ↔ R, G Warburg modulation (indirect) No strong evidence for direct LDH enzyme inhibition; effects likely secondary to survival/redox signaling changes.
9 Migration / invasion (MMPs) MMP2/MMP9 ↓; invasion ↓ (reported) ↔ G Anti-invasive phenotype Reported reduction in metastasis markers in certain systems.
10 Chemo-sensitization (adjunct potential) Therapy sensitivity ↑ (reported in some combinations) Normal tissue protection possible G Adjunct modulation May enhance cytotoxic response in some models; data are preclinical.
11 Translation constraint Clinical anti-cancer efficacy not established Generally well tolerated in dietary contexts — Evidence limitation Human oncology data are limited; dosing and bioavailability remain practical considerations.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (early redox and signaling interactions)
  • R: 30 min–3 hr (NF-κB / PI3K / MAPK modulation)
  • G: >3 hr (apoptosis, angiogenesis, and phenotype-level outcomes)
Casp3, CPP32, Cysteinyl aspartate specific proteinase-3: Click to Expand ⟱
Source:
Type:
Also known as CP32.
Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death.
As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression.
Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy.
Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent.
On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer.
Procaspase-3 is a apoptotic marker protein.
Prognostic significance:
• High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers.
• Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers.
Scientific Papers found: Click to Expand⟱
3631- Cro,    Investigation of the neuroprotective effects of crocin via antioxidant activities in HT22 cells and in mice with Alzheimer's disease
- in-vitro, AD, HT22 - in-vivo, AD, NA
*ROS↓, *Ca+2↓, *BAX↓, *BAD↓, *Casp3↓, *cognitive↑, *memory↑, *Aβ↓, *GPx↑, *SOD↑, *ChAT↑, *Ach↑, *AChE↓, *ROS↓, *p‑Akt↑, *p‑mTOR↑, *neuroP↑,
3630- Cro,    Crocin Improves Cognitive Behavior in Rats with Alzheimer's Disease by Regulating Endoplasmic Reticulum Stress and Apoptosis
- in-vivo, AD, NA
*memory↑, *Bcl-2↑, *BAX↓, *Casp3↓, *GRP78/BiP↓, *CHOP↓, *Dose↝,
3624- Cro,    Crocus Sativus L. (Saffron) in Alzheimer's Disease Treatment: Bioactive Effects on Cognitive Impairment
- Review, AD, NA
*AChE↓, *memory↑, *cognitive↑, *MDA↑, *Thiols↑, *GPx↑, *antiOx↑, *ROS↓, *Casp3↓, *neuroP↑, *SOD↑, *Ach↑, *ChAT↑, *BBB↑, *Aβ↓, *tau↓, *cognitive↑, *Inflam↓,

Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GPx↑, 2,   MDA↑, 1,   ROS↓, 3,   SOD↑, 2,   Thiols↑, 1,  

Cell Death ⓘ

p‑Akt↑, 1,   BAD↓, 1,   BAX↓, 2,   Bcl-2↑, 1,   Casp3↓, 3,  

Transcription & Epigenetics ⓘ

Ach↑, 2,  

Protein Folding & ER Stress ⓘ

CHOP↓, 1,   GRP78/BiP↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑mTOR↑, 1,  

Migration ⓘ

Ca+2↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 2,   ChAT↑, 2,   tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 2,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,  

Functional Outcomes ⓘ

cognitive↑, 3,   memory↑, 3,   neuroP↑, 2,  
Total Targets: 26

Scientific Paper Hit Count for: Casp3, CPP32, Cysteinyl aspartate specific proteinase-3
3 Crocetin
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#:249  Target#:42  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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