Anti-tumor potential of 15,16-dihydrotanshinone I against breast adenocarcinoma through inducing G1 arrest and apoptosis

Tsai, Salina; Suk, Fat Moon; Wang, Chun-I; Liu, Der Zen; Hou, Wen Chi; Lin, Pei Jung; Hung, Ling Fang; Liang, Yu Chih

doi:10.1016/j.bcp.2007.08.009

Cited by 51 publications

(51 citation statements)

References 33 publications

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“…Blocking ASK1 activity by IKK activation may alleviate the effect of poly-Q-induced ER stress. On the other hand, ASK1 also mediates apoptotic cell death triggered by a number of cancer therapeutics through ER stress, elevated ROS, or other mechanisms (28)(29)(30)(31)(32). Therefore, pathways that control ASK1 activity, such as the Akt/IKK signaling axis, are expected to have direct impact on tumor response to therapeutic agents.…”

Section: Discussionmentioning

confidence: 99%

Integration of Apoptosis Signal-Regulating Kinase 1-Mediated Stress Signaling with the Akt/Protein Kinase B-IκB Kinase Cascade

Puckett

Goldman²,

Cockrell³

et al. 2013

Molecular and Cellular Biology

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g Cellular processes are tightly controlled through well-coordinated signaling networks that respond to conflicting cues, such as reactive oxygen species (ROS), endoplasmic reticulum (ER) stress signals, and survival factors to ensure proper cell function. We report here a direct interaction between inhibitor of B kinase (IKK) and apoptosis signal-regulating kinase 1 (ASK1), unveiling a critical node at the junction of survival, inflammation, and stress signaling networks. IKK can be activated by growth factor stimulation or tumor necrosis factor alpha engagement. IKK forms a complex with and phosphorylates ASK1 at a sensor site, Ser967, leading to the recruitment of 14-3-3, counteracts stress signal-triggered ASK1 activation, and suppresses ASK1-mediated functions. An inhibitory role of IKK in JNK signaling has been previously reported to depend on NF-B-mediated gene expression. Our data suggest that IKK has a dual role: a transcription-dependent and a transcription-independent action in controlling the ASK1-JNK axis, coupling IKK to ROS and ER stress response. Direct phosphorylation of ASK1 by IKK also defines a novel IKK phosphorylation motif. Because of the intimate involvement of ASK1 in diverse diseases, the IKK/ASK1 interface offers a promising target for therapeutic development.

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Section: Discussionmentioning

confidence: 99%

Integration of Apoptosis Signal-Regulating Kinase 1-Mediated Stress Signaling with the Akt/Protein Kinase B-IκB Kinase Cascade

Puckett

Goldman²,

Cockrell³

et al. 2013

Molecular and Cellular Biology

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“…Other previous studies and our own showed that DHTS, one of the most effective of the tanshinones, was able to induce apoptosis in a number of human cancer cell lines [15–19], but the exact molecular mechanisms accounting for DHTS-induced apoptosis are not yet fully understood. In this study, we evaluated the activity of DHTS in inhibiting the growth of human prostate carcinoma cells.…”

Section: Discussionmentioning

confidence: 99%

“…Apoptotic cell death was analyzed by flow cytometry using the Annexin V-conjugated Alexa Fluor 488 Apoptosis Detection Kit according the manufacturer's instructions (Molecular Probes, Eugene, OR) [15]. …”

Section: Methodsmentioning

confidence: 99%

“…Recently, other studies and our own found that extracts of tan shen exhibit significant antitumor activity by different mechanisms in various types of tumor cells. We previously showed that DHTS markedly inhibited the proliferation of breast cancer cells through induction of G1-phase arrest and increased loss of the mitochondrial membrane potential and cytochrome c release [15]. Moreover, the inhibitory activity was ranked as follows: DHTS > tanshinone I > cryptotanshinone I. Tanshinone I was also shown to induce cancer cell apoptosis in human myeloid leukemia cells [16] and human nonsmall cell lung cancer [17] whereas tanshinone IIA induced apoptosis in human HeLa [18] and rat glioma cells [19].…”

Section: Introductionmentioning

confidence: 99%

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15,16-Dihydrotanshinone I, a Compound ofSalvia miltiorrhizaBunge, Induces Apoptosis through Inducing Endoplasmic Reticular Stress in Human Prostate Carcinoma Cells

Chuang

et al. 2011

Evidence-Based Complementary and Alternative Medicine

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5,16-dihydrotanshinone I (DHTS) is extracted from Salvia miltiorrhiza Bunge (tanshen root) and was found to be the most effective compound of tanshen extracts against breast cancer cells in our previous studies. However, whether DHTS can induce apoptosis through an endoplasmic reticular (ER) stress pathway was examined herein. In this study, we found that DHTS significantly inhibited the proliferation of human prostate DU145 carcinoma cells and induced apoptosis. DHTS was able to induce ER stress as evidenced by the upregulation of glucose regulation protein 78 (GRP78/Bip) and CAAT/enhancer binding protein homologous protein/growth arrest- and DNA damage-inducible gene 153 (CHOP/GADD153), as well as increases in phosphorylated eukaryotic initiation factor 2α (eIF2α), c-jun N-terminal kinase (JNK), and X-box-binding protein 1 (XBP1) mRNA splicing forms. DHTS treatment also caused significant accumulation of polyubiquitinated proteins and hypoxia-inducible factor (HIF)-1α, indicating that DHTS might be a proteasome inhibitor that is known to induce ER stress or enhance apoptosis caused by the classic ER stress-dependent mechanism. Moreover, DHTS-induced apoptosis was reversed by salubrinal, an ER stress inhibitor. Results suggest that DHTS can induce apoptosis of prostate carcinoma cells via induction of ER stress and/or inhibition of proteasome activity, and may have therapeutic potential for prostate cancer patients.

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“…S. miltiorrhiza has many therapeutic uses to treatment of cardiovascular diseases, hepatitis, inflammation, and cancer (Zhou et al, 2005;Wang, 2010). 15, 16-Dihydrotanshinone Ι (DHT-I) is a constituent of S. miltiorrhiza, and has been reported to have a broad range of biological activities, such as, anti-platelet aggregation (Park et al, 2008), anti-inflammatory (Choi et al, 2004;Lee et al, 2006), anti-tumor (Tsai et al, 2007), and antibacterial activities against a broad range of Gram positive bacteria (Lee et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

15,16-Dihydrotanshinone I suppresses IgE-Ag stimulated mouse bone marrow-derived mast cell activation by inhibiting Syk kinase

Yang

Jin

et al. 2015

Journal of Ethnopharmacology

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Anti-tumor potential of 15,16-dihydrotanshinone I against breast adenocarcinoma through inducing G1 arrest and apoptosis

Cited by 51 publications

References 33 publications

Integration of Apoptosis Signal-Regulating Kinase 1-Mediated Stress Signaling with the Akt/Protein Kinase B-IκB Kinase Cascade

Integration of Apoptosis Signal-Regulating Kinase 1-Mediated Stress Signaling with the Akt/Protein Kinase B-IκB Kinase Cascade

15,16-Dihydrotanshinone I, a Compound ofSalvia miltiorrhizaBunge, Induces Apoptosis through Inducing Endoplasmic Reticular Stress in Human Prostate Carcinoma Cells

15,16-Dihydrotanshinone I suppresses IgE-Ag stimulated mouse bone marrow-derived mast cell activation by inhibiting Syk kinase

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