CRA(Crosolic Acid) isolated from Actinidia valvata Dunn.Radix induces apoptosis of human gastric cancer cell line BGC823 in vitro via down-regulation of the NF-κB pathway

Cheng, Qilai; Li, Hongliang; Li, Yingchen; Liu, Zhao-Wen; Guo, Xiaohua; Cheng, Yi-Jian

doi:10.1016/j.fct.2017.05.021

Cited by 30 publications

(22 citation statements)

References 38 publications

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“…2) Previous studies reported that corosolic acid inhibited the NF-κB signaling pathway in several types of cells. [24][25][26][27] Thus, the down-regulation of ICAM-1 protein expression by corosolic acid appears to be attributed partly to the inhibition of the ICAM-1 mRNA ex- pression or the NF-κB signaling pathway. Corosolic acid is a close structural derivative of ursolic acid, which possesses an extra hydroxyl group at the C-2 position.…”

Section: Discussionmentioning

confidence: 99%

Asiatic Acid, Corosolic Acid, and Maslinic Acid Interfere with Intracellular Trafficking and <i>N</i>-Linked Glycosylation of Intercellular Adhesion Molecule-1

Baba

Hiramatsu

Suradej

et al. 2018

Biological & Pharmaceutical Bulletin

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The pentacyclic triterpenoid ursolic acid was previously shown to inhibit the intracellular trafficking of intercellular adhesion molecule-1 (ICAM-1) from the endoplasmic reticulum (ER) to the Golgi apparatus. In the present study, we further investigated the biological activities of three pentacyclic triterpenoids closely related to ursolic acid on the interleukin 1α-induced expression and intracellular trafficking of ICAM-1. In human lung adenocarcinoma A549 cells, asiatic acid, corosolic acid, and maslinic acid interfered with the intracellular transport of ICAM-1 to the cell surface. Endoglycosidase H-sensitive glycans were linked to ICAM-1 in asiatic acid-, corosolic acid-, and maslinic acid-treated cells. Unlike corosolic acid, asiatic acid and maslinic acid increased the amount of the ICAM-1 protein. Moreover, asiatic acid increased the colocalization of ICAM-1 with calnexin (an ER marker), but not GM130 (a cis-Golgi marker). Asiatic acid, corosolic acid, and maslinic acid inhibited yeast α-glucosidase activity, but not Jack bean α-mannosidase activity. These results indicate that asiatic acid, corosolic acid, and maslinic acid interfere with the intracellular transport of ICAM-1 to the cell surface and cause the accumulation of ICAM-1 linked to endoglycosidase H-sensitive glycans.

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Section: Discussionmentioning

confidence: 99%

Asiatic Acid, Corosolic Acid, and Maslinic Acid Interfere with Intracellular Trafficking and <i>N</i>-Linked Glycosylation of Intercellular Adhesion Molecule-1

Baba

Hiramatsu

Suradej

et al. 2018

Biological & Pharmaceutical Bulletin

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“…It has shown cytotoxic effects in several tumors including cervical cancer [23], hepatocellular carcinoma [18], glioblastoma [21] and lung adenocarcinoma [22], both in vitro and in some tumor xenograft models in vivo. Increasing number of studies showed that CA modulates many cellular signaling events, including Stat-3 [24], nuclear factor-kappa B [25] and Wnt/β-catenin [26]. However, the roles of CA in PCa remain largely unknown, particularly in CRPC.…”

Section: Introductionmentioning

confidence: 99%

Corosolic acid, a natural triterpenoid, induces ER stress-dependent apoptosis in human castration resistant prostate cancer cells via activation of IRE-1/JNK, PERK/CHOP and TRIB3

Zhang

Wang

et al. 2018

J Exp Clin Cancer Res

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BackgroundThe development of potent non-toxic chemotherapeutic drugs against castration resistant prostate cancer (CRPC) remains a major challenge. Corosolic acid (CA), a natural triterpenoid, has anti-cancer activity with limited side effects. However, CA anti-prostate cancer activities and mechanisms, particularly in CRPC, are not clearly understood. In this study, we investigated CA anti-tumor ability against human CRPC and its mechanism of action.MethodsThe cell apoptosis and proliferation effects were evaluated via MTT detection, colony formation assay and flow cytometry. Western blot, gene transfection and immunofluorescence assay were applied to investigate related protein expression of Endoplasmic reticulum stress. A xenograft tumor model was established to investigate the inhibitory effect of CA on castration resistant prostate cancer in vivo.ResultsThe results showed that CA inhibited cell growth and induced apoptosis in human prostate cancer cell (PCa) line PC-3 and DU145, as well as retarded tumor growth in a xenograft model, exerting a limited toxicity to normal cells and tissues. Importantly, CA activated endoplasmic reticulum (ER) stress-associated two pro-apoptotic signaling pathways, as evidenced by increased protein levels of typical ER stress markers including IRE-1/ASK1/JNK and PERK/eIF2α/ATF4/CHOP. IRE-1, PERK or CHOP knockdown partially attenuated CA cytotoxicity against PCa cells. Meanwhile, CHOP induced expression increased Tribbles 3 (TRIB3) level, which lead to AKT inactivation and PCa cell death. CHOP silencing resulted in PCa cells sensitive to CA-induced apoptosis.ConclusionOur data demonstrated, for the first time, that CA might represent a novel drug candidate for the development of an anti-CRPC therapy.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0889-x) contains supplementary material, which is available to authorized users.

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“…From the above cytotoxicity studies, CA has antitumor and antiproliferative activities against many types of human cancer cells, including some murine cancer cells. As listed in Table 1, apoptosis of cancer cells is induced through different molecular mechanisms involving mitochondrial mediation and/or caspase activation [54,56,[58][59][60][61][62]; enhancement of sgnal transducer and activator of transcription 3 (STAT3) and/or nuclear factor-κB [63][64][65]; downregulation of HER2 signaling [66]; activation of AMPK or 5-FU through the inhibition of mammalian target of rapamycin [67,68]; impairment of tumor development by inhibiting the immunosuppressive activity of MDSC [69]; promotion of β-catenin degradation [70]; induction of G2/M cell cycle arrest and downregulation of phosphatidylinositol-3-kinase (PI3K)/Akt signaling [71]; disruption of maternal embryonic leucine zipper kinaseforkhead box M1 signaling [72]; activation of nuclear factor erythroid 2related factor 2 [73]; and targeting the vascular endothelial growth factor receptor 2/steroid receptor coactivator/focal adhesion kinase pathway [74]. Inhibition of Caki renal carcinoma by CA is the only exception as cell death is non-apoptotic caused by the generation of lipid peroxidation and reactive oxygen species [75].…”

Section: Anticancer Propertiesmentioning

confidence: 99%

“…Wong downloaded relevant articles from Science Direct, PubMed, and Google Scholar databases and drafted notes for the manuscript. Enhances the antitumor effects on ovarian carcinoma cells by inhibiting STAT3 and NF-κB [64] BCG823 gastric Induces apoptosis of gastric cancer cells through downregulation of the NF-κB pathway [65] NCI-N87 gastric Downregulates signaling of HER2 which induces cell cycle arrest and apoptosis of gastric cancer cells [66] SNU-601 gastric cancer Activates AMP-activated protein kinase (AMPK) and inhibits mTOR resulting in the growth inhibition and apoptosis of gastric cancer cells [67] SNU-620 gastric carcinoma Enhances the anticancer activities of 5-FU through the inhibition of mTOR in gastric carcinoma cells [68] Murine sarcoma Impairs tumor growth by inhibiting the immunosuppressive activity of MDSC in tumor-bearing mice [69] APC-mutated colon cancer Suppresses proliferation of mutated colon cancer cells through the promotion of β-catenin degradation [70] CaSki cervical cancer Induces apoptosis, G2/M cell cycle arrest, and downregulation of PI3K/Akt signaling in cervical cancer cells [71] Y-79 retinoblastoma Induces cycle arrest and cell apoptosis in retinoblastoma cells through the disruption of MELK-FoxM1 signaling [72] TRAMP-C1 prostate cancer Inhibits the growth of prostate cancer cells by activating Nrf2 [73] Huh7, HepG2, and Hep3B liver carcinoma Inhibits migration of liver carcinoma cells by targeting the VEGFR2/Src/FAK pathway [74] Caki renal carcinoma Induces non-apoptotic cell death through generation of lipid ROS in renal carcinoma cells [75] *…”

Section: Authors' Contributionsmentioning

confidence: 99%

Corosolic Acid: A Synopsis on Its Anticancer Properties

Chan

Wong

2018

Asian J Pharm Clin Res

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Corosolic acid (CA) or 2β-hydroxyursolic acid is an ursane-type pentacyclic triterpene with a molecular formula of C30H48O4 and molecular weight of 473 g/mol. The 30-carbon skeleton and five six-membered rings (A−E) of CA are structurally similar to those of ursolic acid, asiatic acid, and 23-hydroxyl CA. CA was first isolated from the leaf of Lagerstroemia speciosa and later from the fruit of Crataegus pinnatifida. Although L. speciosa (Lythraceae) remains the most important source of CA, Rosaceae and Lamiaceae are the dominant families. This synopsis is focused on the anticancer properties of CA as recent studies have generated new and additional knowledge on its oncology. CA has antitumor, antiproliferative, and apoptotic activities against many types of human cancer cells (including some murine cancer cells), which are inhibited through different molecular mechanisms. Non-apoptotic cell death has also been reported. Depending on the type of cancer cells, the cytotoxicity of CA is comparable to ursolic acid, its analog. Currently, there are no studies on the structure-activity relationship of CA. In ursolic acid, which is structurally similar to CA, the −OH group at C-3 and the −COOH group at C-28 exhibited cytotoxic activity.

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CRA(Crosolic Acid) isolated from Actinidia valvata Dunn.Radix induces apoptosis of human gastric cancer cell line BGC823 in vitro via down-regulation of the NF-κB pathway

Cited by 30 publications

References 38 publications

Asiatic Acid, Corosolic Acid, and Maslinic Acid Interfere with Intracellular Trafficking and <i>N</i>-Linked Glycosylation of Intercellular Adhesion Molecule-1

Asiatic Acid, Corosolic Acid, and Maslinic Acid Interfere with Intracellular Trafficking and <i>N</i>-Linked Glycosylation of Intercellular Adhesion Molecule-1

Corosolic acid, a natural triterpenoid, induces ER stress-dependent apoptosis in human castration resistant prostate cancer cells via activation of IRE-1/JNK, PERK/CHOP and TRIB3

Corosolic Acid: A Synopsis on Its Anticancer Properties

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