Bruceine D induces apoptosis in human non-small cell lung cancer cells through regulating JNK pathway

Tan, Biqin; Huang, Yuyu; Lan, Lihua; Zhang, Bo; Ye, Lijun; Yan, Wei; Wang, Fei; Lin, Nengming

doi:10.1016/j.biopha.2019.109089

Cited by 30 publications

(24 citation statements)

References 26 publications

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“…BD is a quassinoid isolated from the seeds of Brucea javanica, which has been used as a traditional Chinese herb to treat a variety of diseases (Zhang et al, 1980;Shen et al, 2008). Recent studies showed that BD had anti-cancer effect in multiple tumor types, including non-small cell lung cancer (Tan et al, 2019), leukemia (Zhang et al, 2016), osteosarcoma (Wang et al, 2019), hepatocellular carcinoma (Cheng et al, 2017) and pancreatic adenocarcinoma (Lau et al, 2009;Yang et al, 2012). However, as far as we know, the effect of BD in gastric cancer still remains unclear.…”

Section: Discussionmentioning

confidence: 99%

“…BD is also one of these natural compounds extracted from Brucea javanica (Zhang et al, 1980;Shen et al, 2008). Previous studies have demonstrated that BD inhibits the proliferation of non-small cell lung cancer and induces apoptosis mediated by ROS mitochondria and JNK phosphorylation (Tan et al, 2019;Xie et al, 2019). BD inhibits the growth of hepatocellular carcinoma cells by targeting miR-95 (Xiao et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

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Bruceine D inhibits Cell Proliferation Through Downregulating LINC01667/MicroRNA-138-5p/Cyclin E1 Axis in Gastric Cancer

Dong

Shi

et al. 2020

Front. Pharmacol.

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Objective: Gastric cancer is one of the most common malignant tumors. Bruceine D (BD) is one of the extracts of Brucea javanica. In recent years, it has been reported that BD has anti-tumor activity in some human cancers through different mechanisms. Here, this study try to explore the effect of BD on gastric cancer and its regulatory mechanism.Methods: Cell proliferation ability was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assays, 5-bromo-2-deoxyuridine (BrdU) staining and soft agar colony formation assay, respectively. The tumor xenograft model was used to verify the effect of BD on the tumorigenicity of gastric cancer cells in vivo. Flow cytometry analysis and Western blot assay were performed to detect cell cycle and apoptosis. Gastric cancer cells were analyzed by transcriptome sequencing. The interaction between LINC01667, microRNA-138-5p (miR-138-5p) and Cyclin E1 was verified by dual luciferase experiment and RT-PCR assays.Results: We found that BD significantly inhibited cell proliferation and induced cell cycle arrest at S phase in gastric cancer cells. Transcriptome analysis found that the expression of a long non-coding RNA, LINC01667, were significantly down-regulated after BD treatment. Mechanically, it was discovered that LINC01667 upregulated the expression of Cyclin E1 by sponging miR-138-5p. Furthermore, BD enhanced the chemosensitivity of gastric cancer cells to doxorubicin, a clinically used anti-cancer agent.Conclusion: BD inhibit the growth of gastric cancer cells by downregulating the LINC01667/miR-138-5p/Cyclin E1 axis. In addition, BD enhances the chemosensitivity of gastric cancer cells to doxorubicin. This study indicates that BD may be used as a candidate drug for the treatment of patients with gastric cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Bruceine D inhibits Cell Proliferation Through Downregulating LINC01667/MicroRNA-138-5p/Cyclin E1 Axis in Gastric Cancer

Dong

Shi

et al. 2020

Front. Pharmacol.

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“…It is known that dysregulation of cell cycle leading to uncontrolled cell proliferation and apoptosis evasion are hallmarks of all cancer cell types [29,[38][39][40][41]. Indeed, through various cell proliferation assays like Sulforhodamine B assay, MTT assay, and Cell Counting Kit 8 assay, BD has been established to exhibit anti-proliferative properties against pancreatic cancer cells (PANC-1, SW1990, CAPAN-1) [29,37], lung cancer cells [A549, NCI-H292, non-small cell lung cancer (NSCLC) H460] [28,42,43], chronic myeloid leukemia (K562) [44], breast cancer cells (MDA-MB-231) [30], hepatocellular carcinoma cells (Bel7404, HepG2, Hep3B, Huh7, PLC) [45,46], and osteosarcoma cells (MNNG/HOS, U-2OS, MG-63, Saos-2) [47]. In all of the investigated cancer cell lines, there was increased activation of pro-apoptotic proteins like B-cell lymphoma 2 (Bcl-2) associated protein (Bax) and Bak and downregulation of anti-apoptotic proteins like Bcl-2 and myeloid cell leukemia 1 (Mcl-1) [48], all of which are tightly linked to cellular proliferation and apoptotic pathways like phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of Rapamycin (mTOR), c-Jun N-terminal kinase (JNK), mitogen-activated protein kinases (MAPK), and canonical Wnt signaling pathways ( Figure 1) [49][50][51][52].…”

Section: Anti-proliferative and Pro-apoptotic Effects Of Bdmentioning

confidence: 99%

“…NSCLC constitute the majority of lung cancer cases in the world [95][96][97][98][99][100]. The effects of BD on the NSCLC cell lines A549, NCI-H292, and H460 has been investigated by different groups and reported that BD-induced intrinsic cellular apoptosis was mediated through the MAPK/JNK pathway [28,42,43]. Similar to p38-MAPKs, JNKs belong to the MAPK superfamily and regulate important biological processes like cellular proliferation and apoptosis.…”

Section: Effect Of Bd Against Nsclcmentioning

confidence: 99%

A brief overview of antitumoral actions of bruceine D

Sin

Bhardwaj

Pandey

et al. 2020

Exploration of Targeted Anti-Tumor Therapy

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Cancer remains the second leading cause of mortality globally. In combating cancer, conventional chemotherapy and/or radiotherapy are administered as first-line therapy. However, these are usually accompanied with adverse side effects that decrease the quality of patient’s lives. As such, natural bioactive compounds have gained an attraction in the scientific and medical community as evidence of their anticancer properties and attenuation of side effects mounted. In particular, quassinoids have been found to exhibit a plethora of inhibitory activities such as anti-proliferative effects on tumor development and metastasis. Recently, bruceine D, a quassinoid isolated from the shrub Brucea javanica (L.) Merr. (Simaroubaceae), has come under immense investigation on its antineoplastic properties in various human cancers including pancreas, breast, lung, blood, bone, and liver. In this review, we have highlighted the antineoplastic effects of bruceine D and its mode of actions in different tumor models.

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“…Bruceine D (BD) is a natural compound derived from a herb of Brucea javanica. It has been reported that BD has good pharmacological activities including cytotoxic effects on cancer cell, anti-inflammatory and hypoglycemic activities (2,(14)(15)(16)(17). However, little is reported about BD's effects in breast cancer.…”

Section: Introductionmentioning

confidence: 99%

Network-Based Approach to Identify the Antiproliferative Mechanisms of Bruceine D in Breast Cancer From the Cancer Genome Atlas

2020

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Bruceine D (BD) is a natural compound extracted from a Chinese herb Brucea javanica that has been used for anti-inflammatory and anti-cancer treatment. However, little is reported about BD's effects in breast cancer tumorigenesis. In this paper, we aimed to investigate the effect of BD in breast cancer and elucidate the potential mechanism of BD by integrated multiple databases. Our data suggested BD inhibited MCF-7 and MDA-MB-231 cells proliferation and promoted cells apoptosis. We integrated multiple bioinformatics analysis strategies to identify genes, hub modules and pathways associated with BD treatment. Three key pathways, including AMIT_SERUM_RESPONSE_40_MCF10A, BILD_HRAS_ONCOGENIC_SIGNATURE, and NAGASHIMA_NRG1_SIGNALING_UP were identified to be associated with therapeutic effects of BD in breast cancer. Additionally, we validated the key genes by using quantitative real-time PCR and western blot. In conclusion, these findings revealed potential molecular mechanisms of BD to treat breast cancer by affecting AMIT_SERUM_RESPONSE_40_MCF10A, BILD_HRAS_ONCOGENIC_SIGNATURE, and NAGASHIMA_NRG1_SIGNALING_UP pathways and regulating expression of ZFP36, EGR1, and FOS.

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Bruceine D induces apoptosis in human non-small cell lung cancer cells through regulating JNK pathway

Cited by 30 publications

References 26 publications

Bruceine D inhibits Cell Proliferation Through Downregulating LINC01667/MicroRNA-138-5p/Cyclin E1 Axis in Gastric Cancer

Bruceine D inhibits Cell Proliferation Through Downregulating LINC01667/MicroRNA-138-5p/Cyclin E1 Axis in Gastric Cancer

A brief overview of antitumoral actions of bruceine D

Network-Based Approach to Identify the Antiproliferative Mechanisms of Bruceine D in Breast Cancer From the Cancer Genome Atlas

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