PMID- 27910782
OWN - NLM
STAT- MEDLINE
DCOM- 20170207
LR  - 20181202
IS  - 2162-6537 (Electronic)
IS  - 0731-8898 (Linking)
VI  - 35
IP  - 3
DP  - 2016
TI  - Chemoprevention of Colon Cancer through Inhibition of Angiogenesis and Induction 
      of Apoptosis by Nonsteroidal Anti-Inflammatory Drugs.
PG  - 273-289
AB  - Cancer cells require nourishment for the growth of the primary tumor mass and 
      spread of the metastatic colony. These needs are fulfilled by tumor-associated 
      neovasculature known as angiogenesis, which also favors the transition from 
      hyperplasia to neoplasia, that is, from a state of cellular multiplication to 
      uncontrolled proliferation. Therefore, targeting angiogenesis is profitable as a 
      mechanism to inhibit tumor growth. Furthermore, it is important to understand the 
      cross-communication between vascular endothelial growth factor (VEGF) and matrix 
      metalloproteinases (MMPs) in the neoplastic and proinflammatory milieu. We 
      studied the role of two important chemokines (monocyte chemoattractant protein-1 
      [MCP-1] and macrophage inflammatory protein-1beta [MIP-1beta]) along with VEGF and MMPs 
      in nonsteroidal anti-inflammatory drug (NSAID)-induced chemopreventive effects in 
      experimental colon cancer in rats. 1,2-Dimethylhydrazine dihydrochloride (DMH) 
      was used as cancer-inducing agent and three NSAIDs (celecoxib, etoricoxib, and 
      diclofenac) were given orally as chemopreventive agents. Analysis by 
      immunofluorescence and western blotting shows that the expression of VEGF, MMP-2, 
      and MMP-9 was found to be significantly elevated in the DMH- treated group and 
      notably lowered by NSAID coadministration. The expression of MCP-1 was found to 
      be markedly decreased, whereas that of MIP-1beta increased after NSAID 
      coadministration. NSAID coadministration was also able to induce apoptosis, 
      confirmed using studies by Hoechst/propidium iodide (PI) costaining and terminal 
      deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Results from 
      the present study indicate the potential role of these chemokines along with VEGF 
      and MMPs against angiogenesis in DMH-induced cancer. The inhibition of 
      angiogenesis and induction of apoptosis by NSAIDs were found to be possible 
      mechanisms in the chemoprevention of colon cancer.
FAU - Ghanghas, Preety
AU  - Ghanghas P
AD  - Department of Biophysics, Panjab University, Chandigarh, India 160014.
FAU - Jain, Shelly
AU  - Jain S
AD  - Department of Biophysics, Panjab University, Chandigarh, India 160014.
FAU - Rana, Chandan
AU  - Rana C
AD  - Department of Biophysics, Panjab University, Chandigarh, India 160014.
FAU - Sanyal, Sankar Nath
AU  - Sanyal SN
AD  - Department of Biophysics, Panjab University, Chandigarh, India 160014.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Environ Pathol Toxicol Oncol
JT  - Journal of environmental pathology, toxicology and oncology : official organ of 
      the International Society for Environmental Toxicology and Cancer
JID - 8501420
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Anticarcinogenic Agents)
RN  - 0 (Cyclooxygenase 2 Inhibitors)
RN  - 0 (Pyridines)
RN  - 0 (Sulfones)
RN  - 144O8QL0L1 (Diclofenac)
RN  - JCX84Q7J1L (Celecoxib)
RN  - WRX4NFY03R (Etoricoxib)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/*pharmacology/therapeutic use
MH  - Anticarcinogenic Agents/*pharmacology
MH  - Apoptosis/*drug effects
MH  - Celecoxib/pharmacology/therapeutic use
MH  - Colonic Neoplasms/*drug therapy/etiology
MH  - Cyclooxygenase 2 Inhibitors/*pharmacology
MH  - Diclofenac/pharmacology/therapeutic use
MH  - Etoricoxib
MH  - Female
MH  - Neovascularization, Pathologic/*drug therapy/etiology
MH  - Pyridines/pharmacology/therapeutic use
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sulfones/pharmacology/therapeutic use
EDAT- 2016/12/03 06:00
MHDA- 2017/02/09 06:00
CRDT- 2016/12/03 06:00
PHST- 2016/12/03 06:00 [entrez]
PHST- 2016/12/03 06:00 [pubmed]
PHST- 2017/02/09 06:00 [medline]
AID - 2d1506ed13a32809,396d206c5b008734 [pii]
AID - 10.1615/JEnvironPatholToxicolOncol.2016015704 [doi]
PST - ppublish
SO  - J Environ Pathol Toxicol Oncol. 2016;35(3):273-289. doi: 
      10.1615/JEnvironPatholToxicolOncol.2016015704.