Activation of JNK and IRE1 is critically involved in tanshinone I-induced p62 dependent autophagy in malignant pleural mesothelioma cells: implication of p62 UBA domain

Lee, Ji‐Hyun; Sohn, Eun Jung; Yoon, S. Tim; Won, Gunho; Kim, Chang Geun; Jung, Ji Hoon; Kim, Sung Hoon

doi:10.18632/oncotarget.15336

Cited by 19 publications

(19 citation statements)

References 41 publications

(42 reference statements)

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“…2) is a derivative of phenanthrenequinone isolated from the dried root or rhizomes of Salvia miltiorrhiza Bunge. Tanshinone IIA is the primary bioactive constituent of tanshinones [502], which has various pharmacological effects, including anti-inflammatory, anti-cancer and anti-atherosclerotic activities, and cardiovascular protection [503][504][505][506]. Tanshinone exhibits anti-cancer activities in stomach, prostate, lung, breast, and colon cancers, through inducing cell cycle arrest, apoptosis, autophagy, and inhibiting cell migration [507][508][509][510][511][512][513][514][515].…”

Section: Tanshinonesmentioning

confidence: 99%

“…Furthermore, tanshinone IIA induces autophagy to inhibit cell growth in human osteosarcoma 143B and MG63 cells and tumor growth in NOD/SCID mice [526], while it induces autophagy to mediate anticancer activities through activating beclin-1 pathway and inhibiting PI3K/Akt/mTOR pathway in human oral squamous cell carcinoma SCC-9, melanoma A375, and glioma U251 cells [527][528][529]. Moreover, tanshinone IIA is shown to exhibit anti-cancer activities through the interplay between autophagy and apoptosis in human prostate cancer PC-3 cells, mesothelioma H28 and H2452 cells [502,530].…”

Section: Tanshinonesmentioning

confidence: 99%

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Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine

et al. 2019

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Numerous natural products originated from Chinese herbal medicine exhibit anti-cancer activities, including antiproliferative, pro-apoptotic, anti-metastatic, anti-angiogenic effects, as well as regulate autophagy, reverse multidrug resistance, balance immunity, and enhance chemotherapy in vitro and in vivo. To provide new insights into the critical path ahead, we systemically reviewed the most recent advances (reported since 2011) on the key compounds with anti-cancer effects derived from Chinese herbal medicine (curcumin, epigallocatechin gallate, berberine, artemisinin, ginsenoside Rg3, ursolic acid, silibinin, emodin, triptolide, cucurbitacin B, tanshinone I, oridonin, shikonin, gambogic acid, artesunate, wogonin, β-elemene, and cepharanthine) in scientific databases (PubMed, Web of Science, Medline, Scopus, and Clinical Trials). With a broader perspective, we focused on their recently discovered and/or investigated pharmacological effects, novel mechanism of action, relevant clinical studies, and their innovative applications in combined therapy and immunomodulation. In addition, the present review has extended to describe other promising compounds including dihydroartemisinin, ginsenoside Rh2, compound K, cucurbitacins D, E, I, tanshinone IIA and cryptotanshinone in view of their potentials in cancer therapy. Up to now, the evidence about the immunomodulatory effects and clinical trials of natural anti-cancer compounds from Chinese herbal medicine is very limited, and further research is needed to monitor their immunoregulatory effects and explore their mechanisms of action as modulators of immune checkpoints.

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Section: Tanshinonesmentioning

confidence: 99%

Section: Tanshinonesmentioning

confidence: 99%

Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine

et al. 2019

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“…In A375 cells, TA IIA inhibits the proliferation of A375 cells by activating the autophagy pathway [36]. However, Lee et al revealed that TA I induces protective autophagy in malignant pleural mesothelioma cells [37]. Jing et al also revealed that TA I induces pro-survival autophagy in gastric cancers [4].…”

Section: Discussionmentioning

confidence: 99%

Tanshinone I induces cell apoptosis by reactive oxygen species-mediated endoplasmic reticulum stress and by suppressing p53/DRAM-mediated autophagy in human hepatocellular carcinoma

Liu

2020

Artificial Cells, Nanomedicine, and Biotechnology

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“…For example, activation of Jun N-terminal kinase (JNK) was shown to induce p62 mRNA expression [24,25]. In addition, two groups recently reported that inositol-requiring enzyme 1 alpha (IRE1α)/JNK signaling associated with endoplasmic reticulum (ER) stress augments p62 expression [26,27].…”

Section: Introductionmentioning

confidence: 99%

Forced expression of miR-143 and -145 in cardiomyocytes induces cardiomyopathy with a reductive redox shift

et al. 2020

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Background Animal model studies show that reductive stress is involved in cardiomyopathy and myopathy, but the exact physiological relevance remains unknown. In addition, the microRNAs miR-143 and miR-145 have been shown to be upregulated in cardiac diseases, but the underlying mechanisms associated with these regulators have yet to be explored. Methods We developed transgenic mouse lines expressing exogenous miR-143 and miR-145 under the control of the alpha-myosin heavy chain (αMHC) promoter/enhancer. Results The two transgenic lines showed dilated cardiomyopathy-like characteristics and early lethality with markedly increased expression of miR-143. The expression of hexokinase 2 (HK2), a cardioprotective gene that is a target of miR-143, was strongly suppressed in the transgenic hearts, but the in vitro HK activity and adenosine triphosphate (ATP) content were comparable to those observed in wild-type mice. In addition, transgenic complementation of HK2 expression did not reduce mortality rates. Although HK2 is crucial for the pentose phosphate pathway (PPP) and glycolysis, the ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG) was unexpectedly higher in the hearts of transgenic mice. The expression of gamma-glutamylcysteine synthetase heavy subunit (γ-GCSc) and the in vitro activity of glutathione reductase (GR) were also higher, suggesting that the recycling of GSH and its de novo biosynthesis were augmented in transgenic hearts. Furthermore, the expression levels of glucose-6-phosphate dehydrogenase (G6PD, a rate-limiting enzyme for the PPP) and p62/SQSTM1 (a potent inducer of glycolysis and glutathione production) were elevated, while p62/SQSTM1 was upregulated at the mRNA level rather than as a result of autophagy inhibition. Consistent with this observation, nuclear factor erythroid-2 related factor 2 (Nrf2), Jun N-terminal kinase (JNK) and inositol-requiring enzyme 1 alpha (IRE1α) were activated, all of which are known to induce p62/SQSTM1 expression. Conclusions Overexpression of miR-143 and miR-145 leads to a unique dilated cardiomyopathy phenotype with a reductive redox shift despite marked downregulation of HK2 expression. Reductive stress may be involved in a wider range of cardiomyopathies than previously thought.

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Activation of JNK and IRE1 is critically involved in tanshinone I-induced p62 dependent autophagy in malignant pleural mesothelioma cells: implication of p62 UBA domain

Cited by 19 publications

References 41 publications

Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine

Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine

Tanshinone I induces cell apoptosis by reactive oxygen species-mediated endoplasmic reticulum stress and by suppressing p53/DRAM-mediated autophagy in human hepatocellular carcinoma

Forced expression of miR-143 and -145 in cardiomyocytes induces cardiomyopathy with a reductive redox shift

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