Recombinant Methioninase / TumCCA Cancer Research Results

rMETase, Recombinant Methioninase: Click to Expand ⟱
Features:

rMETase - Recombinant Methioninase

Recommended Abbreviation: rMETase

Alternative Names: Recombinant methioninase, recombinant L-methionine α-deamino-γ-mercaptomethane lyase, recombinant methionine γ-lyase

Type: Recombinant enzyme / metabolic anticancer therapy / methionine-depleting biologic

Source: Recombinant methioninase is commonly produced from the Pseudomonas putida methioninase gene expressed in Escherichia coli.

Function: rMETase enzymatically degrades methionine and lowers extracellular and systemic methionine availability. Many cancer cells display methionine dependence or methionine addiction and therefore cannot maintain proliferation when extracellular methionine is depleted, whereas normal cells are generally more capable of compensating through methionine regeneration and related metabolic pathways.

Cancer: Preclinical studies demonstrate broad anticancer activity through methionine depletion, inhibition of proliferation, disruption of methylation-dependent metabolism, and cell-cycle arrest, frequently in late S/G2 phase. rMETase can sensitize cancer cells to chemotherapy and has shown synergistic activity with multiple cytotoxic agents in experimental tumor models.

Clinical Status: Experimental metabolic anticancer therapy. Most evidence is preclinical, although recombinant methioninase has been developed specifically for translational and clinical investigation.
TumCCA, Tumor cell cycle arrest: Click to Expand ⟱
Source:
Type:
Tumor cell cycle arrest refers to the process by which cancer cells stop progressing through the cell cycle, which is the series of phases that a cell goes through to divide and replicate. This arrest can occur at various checkpoints in the cell cycle, including the G1, S, G2, and M phases. S, G1, G2, and M are the four phases of mitosis.
Scientific Papers found: Click to Expand⟱
8033- IVM,  dietMet,  rMETase,    Direct comparison of efficacy of combining ivermectin versus five first-line chemotherapy drugs with recombinant methioninase against colon-cancer cells
- in-vitro, CRC, HCT116
eff↑, ChemoSen↑, eff↑, selectivity↑, eff↑, TumCCA↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   eff↑, 3,   selectivity↑, 1,  
Total Targets: 4

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TumCCA, Tumor cell cycle arrest
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#:473  Target#:322  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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