Neferine inhibits growth and migration of gastrointestinal stromal tumor cell line GIST-T1 by up-regulation of miR-449a

Xue, Fangxi; Li, Zhaoxia; Xu, Jingtao; Xu, Xiaoguang; Chen, Xingtian; Tian, Feng

doi:10.1016/j.biopha.2018.11.029

Cited by 21 publications

(21 citation statements)

References 32 publications

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“…The CSC hypothesis suggests that the elimination of the "root" of cancer is very crucial for curing cancer (Reya, Morrison, Clarke, & Weissman, 2001). Therefore, tar- (Xue et al, 2019), hepatocellular carcinoma (Deng et al, 2017), lung cancer (Poornima, Weng, et al, 2013), breast cancer (Yang et al, 2016), ovarian cancer (Xu et al, 2016), and osteosarcoma cells (Zhang et al, 2012). According to studies on cancer cells, neferine activity varies on tumor cell types.…”

Section: Iscus I Onmentioning

confidence: 99%

“…¢ p < .05 versus untreated (UT). The data are represented as the means ± SD of three independent experiments of GIST cells (Xue et al, 2019). Moreover, the same concentration of neferine does not show antiproliferative effect in normal cells such as hepatocytes (Deng et al, 2017) and retina pigment epithelial cells (Ozal, Gurlu, Turkekul, Guclu, & Erdogan, 2020).…”

Section: Iscus I Onmentioning

confidence: 99%

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Neferine inhibits proliferation and migration of human prostate cancer stem cells through p38 MAPK/JNK activation

Erdoğan

Turkekul

2020

J Food Biochem

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Cancer stem cells (CSCs) are one of the significant causes of cancer treatment failure and metastasis, as they have significant chemo‐and radio‐resistance leading to tumor recurrence. Here we investigated the possible anticancer properties of neferine, a natural alkaloid, on human prostate cancer (PCa) cells and their stem cells. CD44+ CSCs were isolated from androgen‐insensitive PC3 cells by magnetic‐activated cell sorting system (MACS). Neferine dose‐and time‐dependently inhibited the viability of PC3 and CSCs as well as androgen‐sensitive LNCaP cells through inducing apoptosis and cell cycle arrest at G1 phase. Neferine was shown to downregulate the expression of Bcl‐2 and CDK4, and upregulate caspase 3, clePARP, p21, p27, and p53. The treatment significantly inhibits the migration of CSCs. Neferine induces JNK and p38 MAPK phosphorylation, and downregulates PI3K and NF‐ĸβ signaling. In conclusion, neferine may have a therapeutic effect inhibiting the PCa cell proliferation as well as by eliminating CSCs. Practical applications Neferine is an alkaloid found in the seed embryo of Nelumbo nucifera and has recently been shown to have anticancer effects on various human cancer cells. More than 90% of cancer‐related deaths develop after metastasis, and CSCs are considered to be largely responsible for the cell migration and invasion. It has been shown that treatment of neferine kills not only PCa cells but also CSCs, and may contribute to the prevention of progression of PCa and metastasis by inhibiting cell proliferation and migration.

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Section: Iscus I Onmentioning

confidence: 99%

Section: Iscus I Onmentioning

confidence: 99%

Neferine inhibits proliferation and migration of human prostate cancer stem cells through p38 MAPK/JNK activation

Erdoğan

Turkekul

2020

J Food Biochem

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“…Interestingly, a reduced expression of miR‐449a contributed to growth and metastasis of prostate cancer cells by targeting PrLZ . Moreover, antitumor compounds ailanthone and neferine were capable of cascading the production of miR‐449a, thereby suppressing cell growth in acute myeloid leukemia and gastrointestinal stromal cancer . In addition, Zhang et al .…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA SNHG7 contributes to cell proliferation, migration, invasion and epithelial to mesenchymal transition in non‐small cell lung cancer by regulating miR‐449a/TGIF2 axis

et al. 2019

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Background: Non-small cell lung cancer (NSCLC) is an intractable malignant lung cancer with high rates of metastasis and mortality. Currently, long noncoding RNA nuclear RNA host gene 7 (SNHG7) is recognized as a biomarker of multiple cancers. However, the role of SNHG7 in NSCLC requires further understanding. Methods: The expression of SNHG7, miR-449a and TGIF2 in NSCLC tumors and cells was examined by quantitative real time polymerase chain reaction (qRT-PCR). Cell viability was measured by MTT assay. Cell migration and invasion was conducted using transwell assay. Protein expression of TGIF2, vimentin, N-cadherin and E-cadherin was detected by western blot. The interaction between miR-449a and SNHG7 or TGIF2 was determined by luciferase reporter system, RIP and RNA pull-down assay, respectively. Xenograft mice models were established by subcutaneously injecting A549 cells transfected with sh-SNHG7 and sh-control. Results: SNHG7 expression was upregulated in NSCLC tumors and cells compared with normal tissues and cells. SNHG7 silencing repressed cell proliferation, migration, invasion and epithelial to mesenchymal transition (EMT) in NSCLC. Consistently, SNHG7 knockdown hindered tumor growth in vivo. The subsequent luciferase reporter system, RIP and RNA pull-down assay validated the interaction between miR-449a and SNHG7 or TGIF2. The rescue experiments displayed that miR-449a inhibitor counteracted SNHG7 silencing induced inhibition on proliferation, migration, invasion and EMT. Similarly, restoration of TGIF2 reversed miR-449a mediated inhibition on cell progression. In addition, the results indicated that SNHG7 could regulate cell progression by targeting miR-449a/TGIF2 axis. Conclusion: SNHG7 contributed to cell proliferation, migration, invasion and EMT in NSCLC by upregulating TGIF2 via sponging miR-449a, representing a novel targeted therapy method for NSCLC.

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“…The deactivation of Notch and PI3K/AKT signaling pathways was dependent on the upregulation of miR‐449a induced by AIT (Y. Zhang et al, 2019). A few natural products exert similar properties, such as the alkaloid neferine which was found to inhibit growth and migration of gastrointestinal stromal tumor cell line GIST‐T1 by upregulation of miR‐449a (F. Xue et al, 2019).…”

Section: Regulation Of Mi‐rnas Expression and Functionmentioning

confidence: 99%

Anticancer properties and mechanism of action of the quassinoid ailanthone

Bailly

2020

Phytotherapy Research

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Ailanthone (AIT) is a quassinoid natural product isolated from the worldwide‐distributed plant Ailanthus altissima. The drug displays multiple pharmacological properties, in particular significant antitumor effects against a variety of cancer cell lines in vitro. Potent in vivo activities have been evidenced in mice bearing hepatocellular carcinoma, nonsmall cell lung cancer and castration‐resistant prostate cancer. This review focusses on the mechanism of action of AIT, notably to highlight the capacity of the drug to activate DNA damage responses, to inhibit the Hsp90 co‐chaperone p23 and to modulate the expression of several microRNA. The interconnexion between these effects is discussed. The unique capacity of AIT to downregulate oncogenic miR‐21 and to upregulate the tumor suppressor miRNAs miR‐126, miR‐148a, miR‐195, and miR‐449a is presented. AIT exploits several microRNAs to exert its anticancer effects in distinct tumor types. AIT is one of the rare antitumor natural products that binds to and strongly inhibits cochaperone p23, opening interesting perspectives to treat cancers. However, the toxicity profile of the molecule may limit its development as an anticancer drug, unless it can be properly formulated to prevent AIT‐induced gastro‐intestinal damages in particular. The antitumor properties of AIT and analogs are underlined, with the aim to encourage further pharmacological studies with this underexplored natural product and related quassinoids. Highlights Ailanthone (AIT) is an anticancer quassinoid isolated from Ailanthus altissima It inhibits proliferation and induces cell death of many cancer cell types The drug activates DNA damage response and targets p23 cochaperone Up or downregulation of several microRNA by AIT contributes to the anticancer activity Analogs or specific formulations must be developed to prevent the toxicity of AIT

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Neferine inhibits growth and migration of gastrointestinal stromal tumor cell line GIST-T1 by up-regulation of miR-449a

Cited by 21 publications

References 32 publications

Neferine inhibits proliferation and migration of human prostate cancer stem cells through p38 MAPK/JNK activation

Neferine inhibits proliferation and migration of human prostate cancer stem cells through p38 MAPK/JNK activation

Long noncoding RNA SNHG7 contributes to cell proliferation, migration, invasion and epithelial to mesenchymal transition in non‐small cell lung cancer by regulating miR‐449a/TGIF2 axis

Anticancer properties and mechanism of action of the quassinoid ailanthone

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