Trichostatin A and sirtinol suppressed survivin expression through AMPK and p38MAPK in HT29 colon cancer cells

Hsu, Ya Fen; Sheu, Joen Rong; Lin, Chien Huang; Yang, De Shin; Hsiao, George; Ou, George; Chiu, Pei Ting; Huang, Yu Jie; Kuo, Wen Hsin; Hsu, Ming Jen

doi:10.1016/j.bbagen.2011.11.011

Cited by 45 publications

(46 citation statements)

References 45 publications

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“…After activation, p38 MAP kinase plays an important role by targeting various factors including reduction in the expression of survivin and resulting in apoptosis (Hsiao et al, 2007;Hsu et al, 2012). Our results demonstrated that trolox treatment induced activation of p38 in the colon cancer cells.…”

Section: Discussionsupporting

confidence: 50%

Trolox induces inhibition of cell proliferation and apoptosis in human colon cancer cells

Yang¹,

Tian²,

Li³

et al. 2015

Bangladesh J Pharmacol

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In the present study, the effect of trolox on human colon cancer cell lines was investigated. The results revealed that trolox treatment caused inhibition of cell growth in T84 and HCT-15 colon cancer cell lines in a dose-dependent manner. The inhibition was significant at 50 µM of trolox after 48 hours in both cell lines. Trolox treatment promoted expression of p38 and inhibited expression of survivin and Akt. It also induced cleavage of PARP and caspase -3 and ultimately induced apoptosis in T84 and HCT-15 cells. The tumor growth was inhibited significantly in the xenotransplanted mice on treatment with trolox compared to the control group. Since trolox treatment exhibits inhibitory effect on the proliferation of colon cancer cells and inhibits tumor growth in vivo therefore, can be of therapeutic importance for the treatment of colon cancer.

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Section: Discussionsupporting

confidence: 50%

Trolox induces inhibition of cell proliferation and apoptosis in human colon cancer cells

Yang¹,

Tian²,

Li³

et al. 2015

Bangladesh J Pharmacol

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“…However, they are also known to downregulate various genes. HDAC inhibitors were recently reported to suppress the promoter activity of survivin through AMPK and p38MAPK signaling, and Sp1 in colon cancer cells [29]. As shown in Fig.…”

Section: Discussionmentioning

confidence: 86%

The histone deacetylase inhibitor OBP-801 and eribulin synergistically inhibit the growth of triple-negative breast cancer cells with the suppression of survivin, Bcl-xL, and the MAPK pathway

Ono

Sowa

Horinaka

et al. 2018

Breast Cancer Res Treat

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Purpose Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer. Eribulin was approved for the treatment of metastatic breast cancer through the EMBRACE trial, and a subgroup analysis in this clinical trial indicated the efficacy of eribulin in patients with TNBC. However, the prognosis of patients with TNBC is still poor due to various molecular characteristics. Therefore, there is an urgent need for a more effective treatment for the management of TNBC. Methods We investigated the synergistic effect of a novel histone deacetylase (HDAC) inhibitor, OBP-801, and eribulin in TNBC cell lines because OBP-801 has been known to enhance the anti-tumor activities of other chemotherapeutic agents. The cell growth was analyzed, and the flow cytometry analysis was conducted to evaluate the effects on cell cycle and the induction of apoptosis. The mechanism underlying the enhancement of inhibition of TNBC cell growth was investigated through Western blot analyses. Results The combination treatment of OBP-801 with eribulin showed the synergistic inhibition of the growth in TNBC cells, involved with the enhancement of apoptosis. We, for the first time, found that eribulin upregulated survivin and also that OBP-801 could remarkably suppress the upregulation of survivin by eribulin. Moreover, this combination potently suppressed Bcl-xL and the MAPK pathway compared with either agent alone. Conclusion We found that the combination of OBP-801 and eribulin synergistically inhibited the growth with apoptosis in TNBC cells, suggesting that this combination might be a promising novel strategy for treating TNBC patients.

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“…In this context, it is interesting that p38 MAPK, which is a member of the MAPKs family and a stress-responsive MAPK like JNK, appears not to be involved in the ghrelin-stimulated MCP-1 secretion. One of the possible mechanisms is that the inhibition of AMPK activity by ghrelin also, at the same time, diminishes the activity of its downstream kinase, p38 MAPK, because it has been confirmed that the activated AMPK inhibits JNK activity (Miyokawa-Gorin et al, 2012) and, conversely, enhances p38 MAPK (Hsu et al, 2012). On the other hand, ghrelin also increased the phosphorylation of Akt, and interestingly, LY294002, a PI3K inhibitor, obviously attenuated the enhanced VEGF 120 secretion induced by ghrelin, while it exhibited no effects on MCP-1 secretion.…”

Section: Journal Of Cellular Physiology G H R E L I N -S T I M U L a mentioning

confidence: 99%

Ghrelin Augments the Expressions and Secretions of Proinflammatory Adipokines, VEGF₁₂₀ and MCP‐1, in Differentiated 3T3‐L1 Adipocytes

Kitahara

Takahashi

Moriya

et al. 2014

Journal Cellular Physiology

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Ghrelin is a physiological-active peptide with growth hormone-releasing activity, orexigenic activity, etc. In addition, the recent study has also suggested that ghrelin possesses the pathophysiological abilities related to type 2 diabetes. However, the ghrelin-direct-effects implicated in type 2 diabetes on peripheral tissues have been still unclear, whereas its actions on the central nervous system (CNS) appear to induce the development of diabetes. Thus, to assess its peripheral effects correlated with diabetes, we investigated the regulatory mechanisms about adipokines, which play a central role in inducing peripheral insulin resistance, secreted from mature 3T3-L1 adipocytes stimulated with ghrelin in vitro. The stimulation with 50 nmol/L ghrelin for 24 h resulted in the significant 1.9-fold increase on vascular endothelial growth factor-120 (VEGF 120 ) releases (P < 0.01) and the 1.7-fold on monocyte chemoattractant protein-1 (MCP-1) (P < 0.01) from 3T3-L1 adipocytes, respectively, while ghrelin failed to enhance tumor necrosis factor-a (TNF-a), interleukin-1b (IL-1b), IL-6, IL-10 and adiponectin secretions. In addition, Akt phosphorylation on Ser473 and c-Jun NH 2 -terminal protein kinase (JNK) phosphorylation on Thr183/Tyr185 were markedly enhanced 1.4-fold (P < 0.01) and 1.6-fold (P < 0.01) in the ghrelin-stimulated adipocytes, respectively. Furthermore, the treatment with LY294002 (50 mmol/L) and Wortmannin (10nmol/L), inhibitors of phosphatidylinositol 3-kinase (PI3K), significantly decreased the amplified VEGF 120 secretion by 29% (P < 0.01) and 28% (P < 0.01) relative to the cells stimulated by ghrelin alone, respectively, whereas these inhibitors had no effects on increased MCP-1 release. On the other hand, JNK inhibitor SP600125 (10 mmol/L) clearly reduced the increased MCP-1, but not VEGF 120 , release by 35% relative to the only ghrelin-stimulated cells (P < 0.01). In conclusion, ghrelin can enhance the secretions of proinflammatory adipokines, VEGF 120 and MCP-1, but fails to affect IL-10 and adiponectin which are considered to be anti-inflammatory adipokines. Moreover, this augmented VEGF 120 release is invited through the activation of PI3K pathways and the MCP-1 is through JNK pathways. Consequently, our results strongly suggest that ghrelin can induce the development of diabetes via its direct-action in peripheral tissues, as well as, via CNS.

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Trichostatin A and sirtinol suppressed survivin expression through AMPK and p38MAPK in HT29 colon cancer cells

Cited by 45 publications

References 45 publications

Trolox induces inhibition of cell proliferation and apoptosis in human colon cancer cells

Trolox induces inhibition of cell proliferation and apoptosis in human colon cancer cells

The histone deacetylase inhibitor OBP-801 and eribulin synergistically inhibit the growth of triple-negative breast cancer cells with the suppression of survivin, Bcl-xL, and the MAPK pathway

Ghrelin Augments the Expressions and Secretions of Proinflammatory Adipokines, VEGF₁₂₀ and MCP‐1, in Differentiated 3T3‐L1 Adipocytes

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Trichostatin A and sirtinol suppressed survivin expression through AMPK and p38MAPK in HT29 colon cancer cells

Cited by 45 publications

References 45 publications

Trolox induces inhibition of cell proliferation and apoptosis in human colon cancer cells

Trolox induces inhibition of cell proliferation and apoptosis in human colon cancer cells

The histone deacetylase inhibitor OBP-801 and eribulin synergistically inhibit the growth of triple-negative breast cancer cells with the suppression of survivin, Bcl-xL, and the MAPK pathway

Ghrelin Augments the Expressions and Secretions of Proinflammatory Adipokines, VEGF120 and MCP‐1, in Differentiated 3T3‐L1 Adipocytes

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Ghrelin Augments the Expressions and Secretions of Proinflammatory Adipokines, VEGF₁₂₀ and MCP‐1, in Differentiated 3T3‐L1 Adipocytes