Tripterine inhibits proliferation, migration and invasion of breast cancer MDA-MB-231 cells by up-regulating microRNA-15a

Zuo, Anjun; Zhao, Peng; Zheng, Yu; Hua, Hui; Wang, Xingang

doi:10.1515/hsz-2018-0469

Cited by 15 publications

(10 citation statements)

References 36 publications

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“…Tripterine is a plant triterpene, which derives from the root of Thunder of God Vine, has been shown to possess antitumor activities. 5,6,[23][24][25] It has been reported that tripterine represses the growth and metastatic ability of gastric cancer cell MKN45 through down-regulating miRNA-21. 25 In addition, celastrol enhances ovarian cancer cell apoptosis through downregulating miRNA-21 and suppressing the PI3K/AKT/NF-κB signaling axis.…”

Section: Discussionmentioning

confidence: 99%

<p>Tripterine Restrains the Aggressiveness of Hepatocellular Carcinoma Cell via Regulating miRNA-532-5p/CXCL2 Axis</p>

Jiang

Han

Liu

et al. 2020

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Introduction: Triterpene has attracted considerable interests because it exhibits anticancer effects. However, the effects of tripterine on hepatocellular carcinoma (HCC) are not well studied. In the current study, the mechanism of tripterine on HCC cells growth and metastasis was examined. Methods: The inhibitory effect on the growth and aggressiveness in HCC cells was analyzed by Cell Counting Kit-8 (CCK-8), wound healing and Transwell assay. The levels of microRNA-532-5p (miR-532-5p) in HCC cells and tissues were measured using qRT-PCR. The expression of chemokine (C-X-C Motif) ligand 2 (CXCL2) was determined by Western blotting and immunohistochemistry (IHC). Luciferase reporter gene assay was used to validate the binding between miR-532-5p and CXCL2. The impact of tripterine on the growth and metastasis of HCC cells in vivo was analyzed using transplanted tumor model and experimental lung metastasis model, respectively. Results: We found that tripterine inhibited HCC cells proliferation, migration ability and invasion. Under tripterine treatment, the level of miR-532-5p was strikingly raised, and overexpression of miR-532-5p reduced cell viability and metastatic-related traits. In addition, we identified CXCL2 as a target of miR-532-5p in HCC. Rescue experiments indicated that overexpression of CXCL2 restored the migration and invasive capacity of HCC cells inhibited by miR-532-5p or tripterine treatment. Finally, the tumor growth and metastatic ability of HCC MHCC97H cell in vivo were also significantly restrained by tripterine. The expression of CXCL2 was distinctly decreased and miR-532-5p level was increased by tripterine in vivo. Conclusion:In conclusion, tripterine inhibits the growth, migration ability and invasiveness of HCC cells through intervening miR-532-5p/CXCL2.

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Section: Discussionmentioning

confidence: 99%

<p>Tripterine Restrains the Aggressiveness of Hepatocellular Carcinoma Cell via Regulating miRNA-532-5p/CXCL2 Axis</p>

Jiang

Han

Liu

et al. 2020

OTT

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“…The Western blot test showed that cyclin-dependent kinases (CDK1), a cell division associated protein, was lower expressed in si-UBE2C, but the apoptosis-associated factor, Bax, was higher expressed [ 6 ]. The protein level of C-PARP indicated that cell apoptosis was increased after the knockdown of UBE2C under 2 Gy irradiation ( Figure 3A ) [ 10 ]. And Bcl-2, a protein that suppresses apoptosis, was decreased in Si-UBE with 2 Gy irradiation group.…”

Section: Resultsmentioning

confidence: 99%

UBE2C mediated radiotherapy resistance of head and neck squamous cell carcinoma by regulating oxidative-stress-relative apoptosis

Zhou

Zhang

Gong

et al. 2022

Aging

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Purpose: Radiotherapy resistance is the main obstacle in the effective treatment of advanced head and neck squamous cell carcinoma (HNSCC). Increasing scientific opinions present that ubiquitin-conjugating enzyme E2C (UBE2C) might be a target gene acting as an oncogene. Method: TCGA database was used to analyze the expression of UBE2C in HNSCC patients, and the relationship between UBE2C expression and prognosis. Western blot and RT-PCR were used to assess UBE2C expression before and after radiation. Then, cell viability experiment and colony formation were used to evaluate proliferation after 2 Gy radiation. Cell viability experiment, migration, and invasion were evaluated in the condition of UBE2C knock-down. Western blot and RT-PCR were used to assess the expression of apoptosis and ROS relative gene expression. Then, the xenograft model was used to evaluate the efficacy of radiation combined with UBE2C suppression. Result: The expression of UBE2C was high in tumors of patients with HNSCC and relatives with poor prognoses. Si-UBE2C cells showed proliferation inhibited and apoptosis enhanced after radiation. Furthermore, the mechanism of UBE2C in HNSCC radioresistance was explored. We performed RT-PCR to find the 4-HNE, which increases oxidative-stress-relative apoptosis in Si-UBE2C cells after radiation. Conclusions: Through the RT-PCR, WB, cell viability experiment, migration, invasion, and in vivo experiment, UBE2C was confirmed to downregulate oxidative-stress-relative apoptosis induced by radiation and promote the development of malignant tumor cells.

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“…After relevant stimulation and/or treatment, cell apoptosis was tested via Annexin V-FITC/PI Apoptosis Detection Kit (Yeasen Biotechnology, Co., Ltd. Shanghai, China) [ 24 ]. A total of 3 × 10 4 H9c2 cells were cultivated in a 24-well plate for 24 h. Then, cells in each group were gathered, rinsed using PBS, and dyed with 5 μL Annexin V-FITC and 10 μL PI for 15 min protected from light.…”

Section: Methodsmentioning

confidence: 99%

Epigallocatechin-3-gallate protects cardiomyocytes from hypoxia-reoxygenation damage via raising autophagy related 4C expression

et al. 2021

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Myocardial ischemia/reperfusion (I/R) injury is a serious issue during the therapy of myocardial infarction. Herein, we explored the beneficial influence of Epigallocatechin-3-gallate (EGCG) on hypoxia/reoxygenation (H/R)-stimulated cardiomyocyte H9c2 cells damage, along with possible internal molecular mechanism related autophagy related 4C (ATG4C). H9c2 cells were subjected to H/R stimulation and/or EGCG treatment. ATG4C mRNA expression was measured via q-PCR assay. ATG4C overexpression plasmid (OE-ATG4C) was transfected to arise ATG4C level. Cell viability, apoptosis, reactive oxygen species (ROS) production, ATP level were tested via CCK-8 assay, Annexin V-FITC/PI staining, DCFH-DA staining and ATP Assay Kit, respectively. Western blotting was performed to test Cleaved-caspase 3, Cleaved-caspase 9, cytochrome C, and LC3B protein levels. H/R stimulation resulted in H9c2 cell viability loss, promoted cell apoptosis, and ROS overproduction, as well as lowered ATP level in cells. EGCG treatment alleviated H/R-resulted H9c2 cell viability loss, cell apoptosis, ROS overproduction, and reduction of ATP level. Moreover, H/R stimulation reduced the ATG4C expression in H9c2 cells, while EGCG raised the ATG4C expression. Overexpression of ATG4C strengthened the beneficial influence of EGCG on H/R-stimulated H9c2 cell viability, apoptosis and ROS production. Besides, ATG4C overexpression weakened the H/R-stimulated H9c2 cell autophagy via reducing LC3B II/I expression. EGCG exerted beneficial influence on H/R-stimulated cardiomyocytes, which protected cardiomyocytes from H/R-stimulated viability loss, apoptosis, and ROS overproduction via enhancing ATG4C expression.

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Tripterine inhibits proliferation, migration and invasion of breast cancer MDA-MB-231 cells by up-regulating microRNA-15a

Cited by 15 publications

References 36 publications

<p>Tripterine Restrains the Aggressiveness of Hepatocellular Carcinoma Cell via Regulating miRNA-532-5p/CXCL2 Axis</p>

<p>Tripterine Restrains the Aggressiveness of Hepatocellular Carcinoma Cell via Regulating miRNA-532-5p/CXCL2 Axis</p>

UBE2C mediated radiotherapy resistance of head and neck squamous cell carcinoma by regulating oxidative-stress-relative apoptosis

Epigallocatechin-3-gallate protects cardiomyocytes from hypoxia-reoxygenation damage via raising autophagy related 4C expression

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