NDLI: Histone deacetylase inhibitors VPA and TSA induce apoptosis and autophagy in pancreatic cancer cells

Please wait, while we are loading the content...

MicroRNA-145 modulates epithelial-mesenchymal transition and suppresses proliferation, migration and invasion by targeting SIP1 in human cervical cancer cells

HPIP promotes epithelial-mesenchymal transition and cisplatin resistance in ovarian cancer cells through PI3K/AKT pathway activation

CDKN2A-p53 mediated antitumor effect of Lupeol in head and neck cancer

MicroRNA-761 induces aggressive phenotypes in triple-negative breast cancer cells by repressing TRIM29 expression

Histone deacetylase inhibitors VPA and TSA induce apoptosis and autophagy in pancreatic cancer cells

Identification of candidate miRNA biomarkers for pancreatic ductal adenocarcinoma by weighted gene co-expression network analysis

ELMO3 expression indicates a poor prognosis in head and neck squamous cell carcinoma - a short report

Cellular Oncology : Volume 40, Issue 1, February 2017

Cellular Oncology : Volume 39

Cellular Oncology : Volume 38

Cellular Oncology : Volume 37

Cellular Oncology : Volume 36

Cellular Oncology : Volume 35

Cellular Oncology : Volume 34

Histone deacetylase inhibitors VPA and TSA induce apoptosis and autophagy in pancreatic cancer cells

Content Provider	Springer Nature Link
Author	Gilardini Montani, Maria Saveria Granato, Marisa Santoni, Claudio Del Porto, Paola Merendino, Nicolò D’Orazi, Gabriella Faggioni, Alberto Cirone, Mara
Copyright Year	2017
Abstract	Histone deacetylase inhibitors (HDACi) are anti-neoplastic agents that are known to affect the growth of different cancer types, but their underlying mechanisms are still incompletely understood. Here, we compared the effects of two HDACi, i.e., Trichostatin A (TSA) and Valproic Acid (VPA), on the induction of cell death and autophagy in pancreatic cancer-derived cells that exhibit a high metastatic capacity and carry KRAS/p53 double mutations.Cell viability and proliferation tests were carried out using Trypan blue dye exclusion, MTT and BrdU assays. FACS analyses were carried out to assess cell cycle progression, apoptosis, reactive oxygen species (ROS) production and mitochondrial depolarization, while Western blot and immunoprecipitation analyses were employed to detect proteins involved in apoptosis and autophagy.We found that both VPA and TSA can induce apoptosis in Panc1 and PaCa44 pancreatic cancer-derived cells by triggering mitochondrial membrane depolarization, Cytochrome c release and Caspase 3 activation, although VPA was more effective than TSA, especially in Panc1 cells. As underlying molecular events, we found that ERK1/2 was de-phosphorylated and that the c-Myc and mutant p53 protein levels were reduced after VPA and, to a lesser extent, after TSA treatment. Up-regulation of p21 and Puma was also observed, concomitantly with mutant p53 degradation. In addition, we found that in both cell lines VPA increased the pro-apoptotic Bim level, reduced the anti-apoptotic Mcl-1 level and increased ROS production and autophagy, while TSA was able to induce these effects only in PaCA44 cells.From our results we conclude that both VPA and TSA can induce pancreatic cancer cell apoptosis and autophagy. VPA appears have a stronger and broader cytotoxic effect than TSA and, thus, may represent a better choice for anti-pancreatic cancer therapy.
Starting Page	167
Ending Page	180
Page Count	14
File Format	PDF
ISSN	22113428
Journal	Cellular Oncology
Volume Number	40
Issue Number	2
e-ISSN	22113436
Language	English
Publisher	Springer Netherlands
Publisher Date	2017-02-03
Publisher Institution	International Society for Cellular Oncology
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Pancreatic cancer HDACi VPA TSA Apoptosis Autophagy ROS ERK p53 Cancer Research Biomedicine Pathology Oncology
Content Type	Text
Resource Type	Article
Subject	Cancer Research Molecular Medicine Oncology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Histone Deacetylase Inhibitor-Induced Autophagy in Tumor Cells: Implications for p53

Histone deacetylase inhibitors and cell death

Possible Role of Autophagy in the Treatment of Pancreatic Cancer with Histone Deacetylase Inhibitors

Inhibition of histone deacetylases sensitizes glioblastoma cells to lomustine

Glucosidase II beta subunit (GluIIβ) plays a role in autophagy and apoptosis regulation in lung carcinoma cells in a p53-dependent manner

Histone deacetylase inhibitors induce invasion of human melanoma cells in vitro via differential regulation of N-cadherin expression and RhoA activity

Histone deacetylase inhibitors, valproic acid and trichostatin-A induce apoptosis and affect acetylation status of p53 in ERG-positive prostate cancer cells

Restoration of klotho expression induces apoptosis and autophagy in hepatocellular carcinoma cells

Combination Therapy With Histone Deacetylase Inhibitors (HDACi) for the Treatment of Cancer: Achieving the Full Therapeutic Potential of HDACi

Histone deacetylase inhibitors VPA and TSA induce apoptosis and autophagy in pancreatic cancer cells

Similar Documents

Histone Deacetylase Inhibitor-Induced Autophagy in Tumor Cells: Implications for p53

Histone deacetylase inhibitors and cell death

Possible Role of Autophagy in the Treatment of Pancreatic Cancer with Histone Deacetylase Inhibitors

Inhibition of histone deacetylases sensitizes glioblastoma cells to lomustine

Glucosidase II beta subunit (GluIIβ) plays a role in autophagy and apoptosis regulation in lung carcinoma cells in a p53-dependent manner

Histone deacetylase inhibitors induce invasion of human melanoma cells in vitro via differential regulation of N-cadherin expression and RhoA activity

Histone deacetylase inhibitors, valproic acid and trichostatin-A induce apoptosis and affect acetylation status of p53 in ERG-positive prostate cancer cells

Restoration of klotho expression induces apoptosis and autophagy in hepatocellular carcinoma cells

Combination Therapy With Histone Deacetylase Inhibitors (HDACi) for the Treatment of Cancer: Achieving the Full Therapeutic Potential of HDACi

Histone deacetylase inhibitors VPA and TSA induce apoptosis and autophagy in pancreatic cancer cells