Evodiamine inhibits migration and invasion by Sirt1-mediated post-translational modulations in colorectal cancer

Zhou, Peng; Li, Xiaopeng; Jiang, Rong; Chen, Yi; Lv, Xiaoting; Guo, Xing-Xian; Tian, Kuan; Yuan, De-Zhi; Lv, Yanwei; Ran, Jianhua; Li, Jing; Chen, Dilong

doi:10.1097/cad.0000000000000760

Cited by 36 publications

(16 citation statements)

References 33 publications

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“…Upregulation of SIRT1 predicted worse outcome of cervical cancer patients. Knockdown of SIRT1 inhibited the migratory and invasive abilities of colorectal cancer 38. Our findings were in accordant with all the previous findingss, and we discovered miR-29a was participated in the migration, invasion and EMT in cervical cancer through targeting SIRT1.…”

Section: Discussionsupporting

confidence: 92%

<p>MiR-29a function as tumor suppressor in cervical cancer by targeting SIRT1 and predict patient prognosis</p>

Peng

Niu

Wang

et al. 2019

OTT

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IntroductionCervical cancer is the second most frequently malignant tumors in females and metastasis is a challenge of the treatment of cervical cancer. MiR-29a is usually low expressed in several tumors and its functions in cervical cancer remain unclear.Patients and methodsThe quantitative real-time polymerase chain reaction was employed to assess the expression of miR-29a and the Sirtuin-1 (SIRT1). Cell metastatic ability was assessed using Transwell and Western blot assays. The dual-luciferase reporter assay was performed to verify that miR-29a targeted to the 3’-untranslated region (UTR) of SIRT1 mRNA.ResultsMiR-29a was low expressed in cervical cancer and downregulation of miR-29a was associated with poor outcome. MiR-29a regulated the expression of SIRT1 by targeting to its 3’-UTR of mRNA in HeLa cells. SIRT1 was upregulated in cervical cancer tissues and cells in comparison with the non-tumor tissues and normal cells. Upregulation of SIRT1 predicted worse outcome of cervical cancer patients. MiR-29a was participated in the migration, invasion and epithelial–mesenchymal transition (EMT) in cervical cancer through directly targeting to the 3’-UTR of SIRT1 mRNA. SIRT1 reversed partial roles of miR-29a on metastasis in cervical cancer.ConclusionmiR-29a suppressed migration, invasion and EMT by directly targeting to SIRT1 in cervical cancer. The newly identified miR-29a/SIRT1 axis provides novel insight into the pathogenesis of cervical cancer.

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Section: Discussionsupporting

confidence: 92%

<p>MiR-29a function as tumor suppressor in cervical cancer by targeting SIRT1 and predict patient prognosis</p>

Peng

Niu

Wang

et al. 2019

OTT

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“…Herbs containing evodiamine have been used for a long time in East Asia for the treatment of a range of conditions, including digestive problems and pain [29]. Recently, an increasing number of reports have shown that this chemical has significant anti-proliferative and anti-invasive activity in several types of cancer [13,[30][31][32]. We found and reported that evodiamine has selective or superior anti-proliferative activity to the CSCs [13] over the BCCs of breast cancer.…”

Section: Discussionmentioning

confidence: 78%

Evodiamine Eliminates Colon Cancer Stem Cells via Suppressing Notch and Wnt Signaling

Kim

Choi

et al. 2019

Molecules

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Evodiamine, an alkaloid contained in traditional Asian herbal medicines that have been used for hundreds years, is interesting due to its cytotoxic effects against many cancers. We examined the effect of evodiamine on the cancer stem cell (CSC) population and the bulk cultured cancer cells (BCC) of colon cancers to examine the double targeting effect. We found that three colon cancer cell lines’ BCC and CSC are effectively targeted by evodiamine. Evodiamine was able to suppress BCC proliferation and induce apoptosis of the cells captured in G2/M phase, as previously reported. However, evodiamine did not cause the accumulation of CSCs at a certain stage of the cell cycle, resulting in the elimination of stemness through an unknown mechanism. By analyzing the expression of 84 genes related to CSCs in two colon cancer cell lines’ CSC, as well as performing further informatics analyses, and quantitative RT-PCR analyses of 24 CSC genes, we found that evodiamine suppressed the expression of the genes that control key signaling pathways of CSC, namely, WNT and NOTCH signaling, to lead CSC elimination. These results suggest that evodiamine should be further developed for targeting both BCCs and CSCs in colon cancers.

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“…It also ameliorates liver and cardiac fibrosis (Jiang et al, 2017; Yang D. et al, 2018) as well as colitis (Shen et al, 2019). Besides, evodiamine has been reported to have anti-tumor activities: it induces apoptosis in many kinds of tumor cells, including hepatic carcinoma (Qiu et al, 2016), lung cancer (Mohan et al, 2016), colorectal cancer (Zhou et al, 2019), osteosarcoma (Meng et al, 2015), and glioma (Wu et al, 2017), thus preventing their proliferation and migration.…”

Section: Introductionmentioning

confidence: 99%

Evodiamine Augments NLRP3 Inflammasome Activation and Anti-bacterial Responses Through Inducing α-Tubulin Acetylation

Zeng

Chen

et al. 2019

Front. Pharmacol.

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Evodiamine is a major ingredient of the plant Evodia rutaecarpa , which has long been used for treating infection-related diseases including diarrhea, beriberi and oral ulcer, but the underlying mechanism is unclear. Here we aimed to explore whether evodiamine influenced NLRP3 (NLR family, pyrin containing domain 3) inflammasome activation in macrophages, which is a critical mechanism for defending the host against pathogenic infections. We uncovered that evodiamine dose-dependently enhanced NLRP3 inflammasome activation in lipopolysaccharide-primed macrophages, as indicated by increased interleukin (IL)-1β production and caspase-1 cleavage, accompanied by increased ASC speck formation and pyroptosis. Mechanistically, evodiamine induced acetylation of α-tubulin around the microtubule organization center (indicated by γ-tubulin) in lipopolysaccharide-primed macrophages. Such evodiamine-mediated increases in NLRP3 activation and pyroptosis were attenuated by activators of α-tubulin deacetylase, resveratrol and NAD + , or dynein-specific inhibitor ciliobrevin A. Small interfering RNA knockdown of αTAT1 (the gene encoding α-tubulin N -acetyltransferase) expression, which reduced α-tubulin acetylation, also diminished evodiamine-mediated augmentation of NLRP3 activation and pyroptosis. Evodiamine also enhanced NLRP3-mediated production of IL-1β and neutrophil recruitment in vivo . Moreover, evodiamine administration evidently improved survival of mice with lethal bacterial infection, accompanied by increased production of IL-1β and interferon-γ, decreased bacterial load, and dampened liver inflammation. Resveratrol treatment reversed evodiamine-induced increases of IL-1β and interferon-γ, and decreased bacterial clearance in mice. Collectively, our results indicated that evodiamine augmented the NLRP3 inflammasome activation through inducing α-tubulin acetylation, thereby conferring intensified innate immunity against bacterial infection.

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Evodiamine inhibits migration and invasion by Sirt1-mediated post-translational modulations in colorectal cancer

Cited by 36 publications

References 33 publications

<p>MiR-29a function as tumor suppressor in cervical cancer by targeting SIRT1 and predict patient prognosis</p>

<p>MiR-29a function as tumor suppressor in cervical cancer by targeting SIRT1 and predict patient prognosis</p>

Evodiamine Eliminates Colon Cancer Stem Cells via Suppressing Notch and Wnt Signaling

Evodiamine Augments NLRP3 Inflammasome Activation and Anti-bacterial Responses Through Inducing α-Tubulin Acetylation

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