Silencing of RUNX2 enhances gemcitabine sensitivity of p53-deficient human pancreatic cancer AsPC-1 cells through the stimulation of TAp63-mediated cell death

Cell Death Dis. 2015 Oct 15;6(10):e1914. doi: 10.1038/cddis.2015.242.

Authors

H Sugimoto¹, M Nakamura¹, H Yoda², K Hiraoka², K Shinohara², M Sang¹, K Fujiwara³, O Shimozato¹, H Nagase², T Ozaki¹

Affiliations

¹ Laboratory of DNA Damage Signaling, Chiba Cancer Center Research Institute, 666-2 Nitona, Chuou-ku, Chiba 260-8717, Japan.
² Laboratory of Cancer Genetics, Chiba Cancer Center Research Institute, 666-2 Nitona, Chuou-ku, Chiba 260-8717, Japan.
³ Innovative Therapy Research Group, Nihon University Research Institute of Medical Science, Nihon University School of Medicine, 30-1 Oyaguchi-Kamicho, Itabashi, Tokyo 173-8610, Japan.

No abstract available

MeSH terms

Antimetabolites, Antineoplastic / pharmacology*
Apoptosis
Cell Line, Tumor
Core Binding Factor Alpha 1 Subunit / genetics*
Core Binding Factor Alpha 1 Subunit / metabolism
Deoxycytidine / analogs & derivatives*
Deoxycytidine / pharmacology
Drug Resistance, Neoplasm
Gemcitabine
Gene Knockdown Techniques
Humans
Pancreatic Neoplasms / drug therapy
Pancreatic Neoplasms / metabolism
Pancreatic Neoplasms / pathology
Transcription Factors / physiology*
Tumor Suppressor Protein p53 / deficiency
Tumor Suppressor Protein p53 / genetics
Tumor Suppressor Proteins / physiology*

Substances

Antimetabolites, Antineoplastic
Core Binding Factor Alpha 1 Subunit
RUNX2 protein, human
TP53 protein, human
TP63 protein, human
Transcription Factors
Tumor Suppressor Protein p53
Tumor Suppressor Proteins
Deoxycytidine
Gemcitabine