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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Zhijun, Huang Shusheng, Wang Han, Min Jianping, Li Li-Sen, Qin Dechun, Li |
| Description | Author Affiliation: Zhijun H ( Department of Surgery, The First Affiliated Hospital of Soochow University, No. 188, Shi-zi Street, Suzhou, 215000, Jiangsu, People's Republic of China.); Shusheng W ( Department of Surgery, Yancheng First People's Hospital, Yancheng, Jiangsu, People's Republic of China.); Han M ( Center for Translation Medicine, The Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang, China.); Jianping L ( Department of Gastroenterology, Nanjing Medical University Affiliated Suzhou Hospital, Suzhou, China.); Li-Sen Q ( Department of Surgery, The First Affiliated Hospital of Soochow University, No. 188, Shi-zi Street, Suzhou, 215000, Jiangsu, People's Republic of China.); Dechun L ( Department of Surgery, Yancheng First People's Hospital, Yancheng, Jiangsu, People's Republic of China.) |
| Abstract | Histone deacetylase (HDAC) overactivity in colorectal cancer (CRC) promotes cancer progression. In the current study, we showed that 4SC-202, a novel class I HDAC inhibitor (HDACi), potently inhibited survival and proliferation of primary human colon cancer cells and established CRC lines (HT-29, HCT-116, HT-15, and DLD-1). Yet, the same 4SC-202 treatment was non-cytotoxic to colon epithelial cells where HDAC-1/-2 expressions were extremely low. 4SC-202 provoked apoptosis activation in CRC cells, while caspase inhibitors (z-VAD-CHO and z-DVED-CHO) significantly alleviated 4SC-202-exerted cytotoxicity in CRC cells. Meanwhile, 4SC-202 induced dramatic G2-M arrest in CRC cells. Further studies showed that AKT activation might be an important resistance factor of 4SC-202. 4SC-202-induced cytotoxicity was dramatically potentiated with serum starvation, AKT inhibition (by perifosine or MK-2206), or AKT1-shRNA knockdown in CRC cells. On the other hand, exogenous expression of constitutively active AKT1 (CA-AKT1) decreased the sensitivity by 4SC-202 in HT-29 cells. Notably, 4SC-202, at a low concentration, enhanced oxaliplatin-induced in vitro anti-CRC activity. In vivo, we showed that oral gavage of 4SC-202 inhibited HT-29 xenograft growth in nude mice, and when combined with oxaliplatin, its activity was further strengthened. Together, these pre-clinical results indicate that 4SC-202 may be further investigated as a valuable anti-CRC agent/chemo-adjuvant. |
| File Format | HTM / HTML |
| ISSN | 10104283 |
| Issue Number | 8 |
| Journal | Tumor Biology |
| Volume Number | 37 |
| e-ISSN | 14230380 |
| Language | English |
| Publisher | Springer |
| Publisher Date | 2016-08-01 |
| Publisher Place | Netherlands |
| Access Restriction | Subscribed |
| Content Type | Text |
| Resource Type | Article |
| Subject | Medicine Cancer Research |
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