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Metformin augments doxorubicin cytotoxicity in mammary carcinoma through activation of adenosine monophosphate protein kinase pathway.

Abstract Since the incidence of breast cancer increases dramatically all over the world, the search for effective treatment is an urgent need. Metformin has demonstrated anti-tumorigenic effect both in vivo and in vitro in different cancer types. This work was designed to examine on molecular level the mode of action of metformin in mice bearing solid Ehrlich carcinoma and to evaluate the use of metformin in conjunction with doxorubicin as a combined therapy against solid Ehrlich carcinoma. Ehrlich ascites carcinoma cells were inoculated in 60 female mice as a model of breast cancer. The mice were divided into four equal groups: Control tumor, metformin, doxorubicin, and co-treatment. Metformin (15 mg/kg) and doxorubicin (4 mg/kg) were given intraperitoneally (i.p.) for four cycles every 5 days starting on day 12 of inoculation. The anti-tumorigenic effect of metformin was mediated by enhancement of adenosine monophosphate protein kinase activity and elevation of P53 protein as well as the suppression of nuclear factor-kappa B, DNA contents, and cyclin D1 gene expression. Metformin and doxorubicin mono-treatments exhibited opposing action regarding cyclin D1 gene expression, phosphorylated adenosine monophosphate protein kinase, and nuclear factor-kappa B levels. Co-treatment markedly decreased tumor volume, increased survival rate, and improved other parameters compared to doxorubicin group. In parallel, the histopathological findings demonstrated enhanced apoptosis and absence of necrosis in tumor tissue of co-treatment group. Metformin proved chemotherapeutic effect which could be mediated by the activation of adenosine monophosphate protein kinase and related pathways. Combining metformin and doxorubicin, which exhibited different mechanisms of action, produced greater efficacy as anticancer therapeutic regimen.
PMID
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Authors

Mayor MeshTerms
Keywords

Cyclin D1

doxorubicin

metformin

nuclear factor-kappa B

solid Ehrlich carcinoma

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28459206
OWN - NLM
STAT- In-Process
DA  - 20170501
LR  - 20170501
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 5
DP  - 2017 May
TI  - Metformin augments doxorubicin cytotoxicity in mammary carcinoma through
      activation of adenosine monophosphate protein kinase pathway.
PG  - 1010428317692235
LID - 10.1177/1010428317692235 [doi]
AB  - Since the incidence of breast cancer increases dramatically all over the world,
      the search for effective treatment is an urgent need. Metformin has demonstrated 
      anti-tumorigenic effect both in vivo and in vitro in different cancer types. This
      work was designed to examine on molecular level the mode of action of metformin
      in mice bearing solid Ehrlich carcinoma and to evaluate the use of metformin in
      conjunction with doxorubicin as a combined therapy against solid Ehrlich
      carcinoma. Ehrlich ascites carcinoma cells were inoculated in 60 female mice as a
      model of breast cancer. The mice were divided into four equal groups: Control
      tumor, metformin, doxorubicin, and co-treatment. Metformin (15 mg/kg) and
      doxorubicin (4 mg/kg) were given intraperitoneally (i.p.) for four cycles every 5
      days starting on day 12 of inoculation. The anti-tumorigenic effect of metformin 
      was mediated by enhancement of adenosine monophosphate protein kinase activity
      and elevation of P53 protein as well as the suppression of nuclear factor-kappa
      B, DNA contents, and cyclin D1 gene expression. Metformin and doxorubicin
      mono-treatments exhibited opposing action regarding cyclin D1 gene expression,
      phosphorylated adenosine monophosphate protein kinase, and nuclear factor-kappa B
      levels. Co-treatment markedly decreased tumor volume, increased survival rate,
      and improved other parameters compared to doxorubicin group. In parallel, the
      histopathological findings demonstrated enhanced apoptosis and absence of
      necrosis in tumor tissue of co-treatment group. Metformin proved chemotherapeutic
      effect which could be mediated by the activation of adenosine monophosphate
      protein kinase and related pathways. Combining metformin and doxorubicin, which
      exhibited different mechanisms of action, produced greater efficacy as anticancer
      therapeutic regimen.
FAU - El-Ashmawy, Nahla E
AU  - El-Ashmawy NE
AD  - Department of Biochemistry, Faculty of Pharmacy, Tanta University, Tanta, Egypt.
FAU - Khedr, Naglaa F
AU  - Khedr NF
AD  - Department of Biochemistry, Faculty of Pharmacy, Tanta University, Tanta, Egypt.
FAU - El-Bahrawy, Hoda A
AU  - El-Bahrawy HA
AD  - Department of Biochemistry, Faculty of Pharmacy, Tanta University, Tanta, Egypt.
FAU - Abo Mansour, Hend E
AU  - Abo Mansour HE
AD  - Department of Biochemistry, Faculty of Pharmacy, Tanta University, Tanta, Egypt.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
OTO - NOTNLM
OT  - Cyclin D1
OT  - doxorubicin
OT  - metformin
OT  - nuclear factor-kappa B
OT  - solid Ehrlich carcinoma
EDAT- 2017/05/02 06:00
MHDA- 2017/05/02 06:00
CRDT- 2017/05/02 06:00
AID - 10.1177/1010428317692235 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 May;39(5):1010428317692235. doi: 10.1177/1010428317692235.

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