The Effect of Gemcitabine on Cell Cycle Arrest and microRNA Signatures in Pancreatic Cancer Cells.


Journal

In vivo (Athens, Greece)
ISSN: 1791-7549
Titre abrégé: In Vivo
Pays: Greece
ID NLM: 8806809

Informations de publication

Date de publication:
Historique:
received: 28 05 2020
revised: 24 07 2020
accepted: 27 07 2020
entrez: 4 11 2020
pubmed: 5 11 2020
medline: 22 6 2021
Statut: ppublish

Résumé

Gemcitabine, an inhibitor of DNA synthesis, is the gold standard chemotherapeutic agent for pancreatic ductal adenocarcinoma (PDAC). MicroRNAs (miRNAs) play critical roles in cancers, including PDAC. However, less is known about the effect of gemcitabine on PDAC cells and miRNA expression in PDAC. We evaluated the effect of gemcitabine on the cell cycle of PDAC cells in vitro and in vivo and on the miRNA expression profile. Effects of gemcitabine on PK-1 and PK-9 cell growth were evaluated using a cell counting kit-8 assay. Xenografted mouse models were used to assess gemcitabine effects in vivo. Gemcitabine inhibited the proliferation and tumour growth of PK-1 cells, and induced S phase cell cycle arrest. Numerous miRNAs were altered upon gemcitabine treatment of PK-1 cells and xenograft models. Altered miRNAs may serve as potential therapeutic targets for improving the efficacy of gemcitabine in PDAC.

Sections du résumé

BACKGROUND/AIM OBJECTIVE
Gemcitabine, an inhibitor of DNA synthesis, is the gold standard chemotherapeutic agent for pancreatic ductal adenocarcinoma (PDAC). MicroRNAs (miRNAs) play critical roles in cancers, including PDAC. However, less is known about the effect of gemcitabine on PDAC cells and miRNA expression in PDAC. We evaluated the effect of gemcitabine on the cell cycle of PDAC cells in vitro and in vivo and on the miRNA expression profile.
MATERIALS AND METHODS METHODS
Effects of gemcitabine on PK-1 and PK-9 cell growth were evaluated using a cell counting kit-8 assay. Xenografted mouse models were used to assess gemcitabine effects in vivo.
RESULTS RESULTS
Gemcitabine inhibited the proliferation and tumour growth of PK-1 cells, and induced S phase cell cycle arrest. Numerous miRNAs were altered upon gemcitabine treatment of PK-1 cells and xenograft models.
CONCLUSION CONCLUSIONS
Altered miRNAs may serve as potential therapeutic targets for improving the efficacy of gemcitabine in PDAC.

Identifiants

pubmed: 33144424
pii: 34/6/3195
doi: 10.21873/invivo.12155
pmc: PMC7811671
doi:

Substances chimiques

MicroRNAs 0
Deoxycytidine 0W860991D6
Gemcitabine 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3195-3203

Informations de copyright

Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

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Auteurs

Daisuke Namima (D)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Shintaro Fujihara (S)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Hisakazu Iwama (H)

Life Science Research Center, Kagawa University, Kagawa, Japan.

Koji Fujita (K)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Takanori Matsui (T)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Mai Nakahara (M)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Megumi Okamura (M)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Masahiro Hirata (M)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Toshiaki Kono (T)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Naoki Fujita (N)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Hiroki Yamana (H)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Kiyohito Kato (K)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Hideki Kamada (H)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Asahiro Morishita (A)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Hideki Kobara (H)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.

Kunihiko Tsutsui (K)

Life Science Research Center, Kagawa University, Kagawa, Japan.

Tsutomu Masaki (T)

Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan tmasaki@med.kagawa-u.ac.jp.

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