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Research
JianWei Jiang
Jinan University
Corresponding Author
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Background
Previous studies have indicated that harmine hydrochloride (HAR-HC) has anti-tumor characteristics. However, its potential impact on human leukemia cells is unknown. In this study, we explored the potential mechanism of HAR-HC effects on human leukemia cells in vitro.
Methods
MTT assay was used to detect cell viability; A flow cytometer was used to analyze the cell cycle; Anexinn V-FITC/PI was used to detect cell apoptosis; Western blotting assay was used to analyze the expression of related proteins.
Results
The result of flow cytometry suggested G2/M phage arrest in K562 cells induced by HAR-HC. The expression levels of Cyclin E2, Cyclin D1, Bcl-2, Bcl-xL, Mcl-1, pro-caspase-3, and PARP decreased and the expression levels of Cyclin A2, Cyclin B1, p21, Myt-1, p-cdc2 (Tyr15), cleaved -caspase-3 and cleaved-PARP increased. Moreover, the expression of p-JNK and p-ERK1/2 increased and autophagy was induced in the HAR-HC treatment group. Additionally, HAR-HC facilitated autophagy by activating the ERK1/2 pathway.
Conclusion
HAR-HC induced G2/M phase cell cycle arrest, autophagy and apoptosis by activating the JNK, and ERK1/2 pathways in the human leukemia K562 cells.
Keywords
Harmine hydrochloride, cell cycle, autophagy, apoptosis, ERK1/2
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A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
JianWei Jiang
Jinan University
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 15 Feb, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Previous studies have indicated that harmine hydrochloride (HAR-HC) has anti-tumor characteristics. However, its potential impact on human leukemia cells is unknown. In this study, we explored the potential mechanism of HAR-HC effects on human leukemia cells in vitro.
Methods
MTT assay was used to detect cell viability; A flow cytometer was used to analyze the cell cycle; Anexinn V-FITC/PI was used to detect cell apoptosis; Western blotting assay was used to analyze the expression of related proteins.
Results
The result of flow cytometry suggested G2/M phage arrest in K562 cells induced by HAR-HC. The expression levels of Cyclin E2, Cyclin D1, Bcl-2, Bcl-xL, Mcl-1, pro-caspase-3, and PARP decreased and the expression levels of Cyclin A2, Cyclin B1, p21, Myt-1, p-cdc2 (Tyr15), cleaved -caspase-3 and cleaved-PARP increased. Moreover, the expression of p-JNK and p-ERK1/2 increased and autophagy was induced in the HAR-HC treatment group. Additionally, HAR-HC facilitated autophagy by activating the ERK1/2 pathway.
Conclusion
HAR-HC induced G2/M phase cell cycle arrest, autophagy and apoptosis by activating the JNK, and ERK1/2 pathways in the human leukemia K562 cells.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
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