PMID- 30806292
OWN - NLM
STAT- MEDLINE
DCOM- 20190321
LR  - 20190321
IS  - 2162-6537 (Electronic)
IS  - 0731-8898 (Linking)
VI  - 38
IP  - 1
DP  - 2019
TI  - PI3K/Akt Pathway and miR-21 are Involved in N-Ethyl-N-Nitrosourea-Induced F1 
      Mouse Lung Tumorigenesis: Effect of Inositol Hexaphosphate.
PG  - 69-81
LID - 10.1615/JEnvironPatholToxicolOncol.2018026684 [doi]
AB  - The risk of cancer development in offspring due to carcinogen exposure during 
      pregnancy is a serious issue. In this study, we explored the involvement of the 
      phosphatidylinositol 3-kinase (PI3K)/Akt pathway and microRNA-21 (miR-21) in 
      transplacental lung tumorigenesis and its prevention by dietary compound inositol 
      hexaphosphate (IP6) in F1 mice. Balb/c mice were exposed to the 
      N-ethyl-N-nitrosourea (ENU) intraperitoneally on the 17th day of gestation. After 
      weaning, half of the litters were fed with oral 2% IP6. At the end of 30, 120, or 
      240 days, we did not observe any effect on fetal viability or weight between 
      ENU-exposed and non-exposed litters and the same was true of IP6. Altered 
      expressions of the PI3K/Akt pathway were observed in F1 mice. Further, miR-21 
      expressions were found to be modulated at the respective time as well, along with 
      the activation of matrix metalloproteinase (MMP-9) and vascular endothelial 
      growth factor expression. Akt activation also enhanced the expression of cyclin 
      D1, cyclooxygenase-2 (COX-2), nuclear factor-kappaB (NF-kappaBp50), and mammalian target 
      of rapamycin (mTOR). IP6-fed F1 mice showed reduced tumorigenesis along with 
      reduced expression of the PI3K/Akt pathway miR-21 and downstream targets. The 
      PI3K/Akt pathway and miR-21 are involved in transplacental lung tumorigenesis, 
      whereas IP6 seemed to affect lung tumorigenesis by suppressing the expression of 
      the PI3K/Akt pathway in F1 mice.
FAU - Sahay, Satya
AU  - Sahay S
AD  - Environmental Carcinogenesis Laboratory Council of Scientific and Industrial 
      Research (CSIR)-Indian Institute of Toxicology Research (IITR), Mahatma Gandhi 
      Marg, Lucknow 226001, India.
FAU - Tiwari, Prakash
AU  - Tiwari P
AD  - Environmental Carcinogenesis Laboratory Council of Scientific and Industrial 
      Research (CSIR)-Indian Institute of Toxicology Research (IITR), Mahatma Gandhi 
      Marg, Lucknow 226001, India.
FAU - Pandey, Manuraj
AU  - Pandey M
AD  - Environmental Carcinogenesis Laboratory Council of Scientific and Industrial 
      Research (CSIR)-Indian Institute of Toxicology Research (IITR), Mahatma Gandhi 
      Marg, Lucknow 226001, India.
FAU - Gupta, Krishna P
AU  - Gupta KP
AD  - Environmental Carcinogenesis Laboratory Council of Scientific and Industrial 
      Research (CSIR)-Indian Institute of Toxicology Research (IITR), Mahatma Gandhi 
      Marg, Lucknow 226001, India.
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 (MIRN21 microRNA, mouse)
RN  - 0 (MicroRNAs)
RN  - 7IGF0S7R8I (Phytic Acid)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Animals
MH  - Carcinogenesis/drug effects/genetics
MH  - Female
MH  - Lung Neoplasms/*metabolism/pathology
MH  - Mice, Inbred BALB C
MH  - MicroRNAs/metabolism/*physiology
MH  - Phosphatidylinositol 3-Kinases/metabolism/*physiology
MH  - Phytic Acid/*pharmacology
MH  - Proto-Oncogene Proteins c-akt/metabolism/*physiology
EDAT- 2019/02/27 06:00
MHDA- 2019/03/22 06:00
CRDT- 2019/02/27 06:00
PHST- 2019/02/27 06:00 [entrez]
PHST- 2019/02/27 06:00 [pubmed]
PHST- 2019/03/22 06:00 [medline]
AID - 4b309b253eb144f8,59b97b3b134afa39 [pii]
AID - 10.1615/JEnvironPatholToxicolOncol.2018026684 [doi]
PST - ppublish
SO  - J Environ Pathol Toxicol Oncol. 2019;38(1):69-81. doi: 
      10.1615/JEnvironPatholToxicolOncol.2018026684.