Potentiation of the anticancer effect of doxorubicinin drug-resistant gastric cancer cells by tanshinone IIA

Xu, Zhenyu; Chen, Lu; Xiao, Zhangang; Zhu, Yanhong; Jiang, Hui; Jin, Yan; Gu, Cheng; Wu, Yilai; Wang, Lin; Zhang, Wen; Zuo, Jian; Zhou, Dexi; Luan, Jiajie; Shen, Jing

doi:10.1016/j.phymed.2018.05.012

Cited by 71 publications

(62 citation statements)

References 30 publications

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“…As one of the main active components of Salvia miltiorrhiza, Tanshinone IIA (TSA) has been found effective in many diseases, such as cardiovascular diseases, liver diseases, and cancer [6][7][8]. TSA has been broadly studied for its multiple pharmacological properties including antiangiogenic, antioxidant, anti-inflammatory, and anticancer activities [7,9,10]. More importantly, its sulfonate sodium injection has been clinically applied in China for many years, especially in cardiovascular and cerebrovascular diseases.…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA Protects against Acute Pancreatitis in Mice by Inhibiting Oxidative Stress via the Nrf2/ROS Pathway

Chen

Yuan

Lǚ

et al. 2020

Oxidative Medicine and Cellular Longevity

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Background. Danshen (Salvia miltiorrhiza Bunge) and its main active component Tanshinone IIA (TSA) are clinically used in China. However, the effects of TSA on acute pancreatitis (AP) and its potential mechanism have not been investigated. In this study, our objective was to investigate the protective effects of TSA against AP via three classic mouse models. Methods. Mouse models of AP were established by caerulein, sodium taurocholate, and L-arginine, separately. Pancreatic and pulmonary histopathological characteristics and serum amylase and lipase levels were evaluated, and changes in oxidative stress injury and the ultrastructure of acinar cells were observed. The reactive oxygen species (ROS) inhibitor N-Acetylcysteine (NAC) and nuclear factor erythroid 2-related factor 2 (Nrf2) knockout mice were applied to clarify the protective mechanism of the drug. Results. In the caerulein-induced AP model, TSA administration reduced serum amylase and lipase levels and ameliorated the histopathological manifestations of AP in pancreatic tissue. Additionally, TSA appreciably decreased ROS release, protected the structures of mitochondria and the endoplasmic reticulum, and increased the protein expression of Nrf2 and heme oxygenase 1 of pancreatic tissue. In addition, the protective effects of TSA against AP were counteracted by blocking the oxidative stress (NAC administration and Nrf2 knockout in mice). Furthermore, we found that TSA protects pancreatic tissue from damage and pancreatitis-associated lung injury in two additional mouse models induced by sodium taurocholate and by L-arginine. Conclusion. Our data confirmed the protective effects of TSA against AP in mice by inhibiting oxidative stress via the Nrf2/ROS pathway.

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Section: Introductionmentioning

confidence: 99%

Tanshinone IIA Protects against Acute Pancreatitis in Mice by Inhibiting Oxidative Stress via the Nrf2/ROS Pathway

Chen

Yuan

Lǚ

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Tan IIA exhibits antineoplastic activity in a variety of malignancies, such as hepatic (35), gastric (36) and colorectal cancer (37), although the underlying mechanism has not been determined. In our previous studies (10,11), high-doses of Tan IIA significantly inhibited proliferation in CRC cells and decreased VEGF expression through regulation of COX-2 expression.…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA reduces secretion of pro‑angiogenic factors and inhibits angiogenesis in human colorectal cancer

et al. 2020

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Tumor angiogenesis is an important factor which precipitates recurrence and metastasis of colorectal cancer (CRC). Angiogenesis is also a significant feature which accompanies invasion and metastasis of CRC. Tumor hypoxia activates hypoxia inducible factor (HIF), which promotes angiogenesis in CRC. HIF significantly promotes cell proliferation and angiogenesis in CRC, facilitating invasion and metastasis. Tanshinone IIA (Tan IIA) has been revealed to effectively inhibit angiogenesis in CRC, although the underlying mechanism remains to be determined. The aim of the present study was to determine the effects of HIF-1α on hypoxia induced angiogenesis in CRC cells, the effects of Tan IIA on the expression of pro-angiogenic factors in CRC cells, and on human umbilical vein endothelial cell (HUVEC) tube formation in normal and hypoxic conditions. The results of the present study revealed that Tan IIA not only decreased HIF-1α expression and inhibited the secretion level of vascular endothelial growth factor and basic fibroblast growth factor, but also efficiently decreased proliferation, tube formation and metastasis of HUVECs. The results highlight the potential of Tan IIA-mediated targeting of HIF-1α as a potential therapeutic option for treatment of patients with CRC.

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“…With regard to gastric cancer, it was found that tanshinone IIA reinforced antineoplastic effect in doxorubicin-resistant gastric cancer cell lines SNU-719R and SNU-610R. The inhibition of multidrug resistanceassociated protein 1 was verified to increase apoptosis and induce autophagic cell death, which contributed to the potent anticancer effect of tanshinone IIA in doxorubicin-resistant gastric cancer cells [66].…”

Section: Chinese Herbal Medicine That Is Favorable In Reducing the Drmentioning

confidence: 94%

The Underlying Mechanisms of Chinese Herbal Medicine-Induced Apoptotic Cell Death in Human Cancer

Chen¹,

Zhong²,

Tan³

et al. 2020

Programmed Cell Death

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The high incidence of cancer is a global burden. Cancer cells acquire immortality, which results in loss of control in cell proliferation and population expansion. Cancer cells undergo a series of genomic instability, leading to mutated amplification or deletion of certain genes that strictly control the cell fate. Programmed cell death is a mechanism of cell fate control that is aberrantly regulated in cancer cells. Apoptosis is the major form of programmed cell death regulated by both intrinsic and extrinsic pathways. Discovering effective and specific alternative solutions that can reprogram apoptosis in cancer cells is always a challenge. Chinese herbal medicine has captured increasing attention from both researchers and manufacturers, as evidenced by observable curative effects from previous clinical experience. Hence, to clarify and reinforce the understanding of the effect of Chinese medicine on cancer, in this chapter, we will retrospectively review the latest 5 years of literature and summarize the mode of action of Chinese herbal medicine on apoptotic cell death in cancer. Both Chinese medicine-induced intrinsic and extrinsic mechanisms of apoptosis will be discussed, and common compounds from Chinese medicine with druggable potential as novel apoptosis-inducing agents will be highlighted.

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Potentiation of the anticancer effect of doxorubicinin drug-resistant gastric cancer cells by tanshinone IIA

Cited by 71 publications

References 30 publications

Tanshinone IIA Protects against Acute Pancreatitis in Mice by Inhibiting Oxidative Stress via the Nrf2/ROS Pathway

Tanshinone IIA Protects against Acute Pancreatitis in Mice by Inhibiting Oxidative Stress via the Nrf2/ROS Pathway

Tanshinone IIA reduces secretion of pro‑angiogenic factors and inhibits angiogenesis in human colorectal cancer

The Underlying Mechanisms of Chinese Herbal Medicine-Induced Apoptotic Cell Death in Human Cancer

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