Aim: To investigate the effects of Hax-1 siRNA on sensitivity to chemotherapy of melanoma A375 cells.
Methods: The effects of Hax-1 siRNA combined with cisplatin(DDP) or Matrine(Mat) on proliferation, apoptosis of A375 cells and active forms of caspase-3 were detected with MTT assay, Annexin V-FITC/PI staining with FCM, Hoechst 33258 staining, and Western blot respectively.
Results: The inhibition of proliferation , induction of apoptosis and the expression of active caspase-3 forms in DDP or Mat treated A375 cells transfected with Hax-1 siRNA were all significantly higher than those in untransfected A375 cells or A375 cells transfected with control siRNA (P<0.05). The distinctive apoptotic morphology was observed in Mat or DDP treated A375 cells transfected with Hax-1 siRNA.
Conclusion: The data from our current study indicate that Hax-1 siRNA could enhance the effects of DDP or Mat on inhibition of melanoma A375 cell growth and induction apoptosis, which may be caused by the increased expression of active forms of caspase-3.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Neuroprotective roles of HAX-1 in ischemic neuronal injury.
Exp Neurol
May 2021
Department of Neurosurgery, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Yamanashi, Japan.
Hematopoietic cell-specific protein 1 associated protein X-1 (HAX-1) is a novel mitochondrial protein that regulates oxidative stress-induced apoptosis. However, the roles of HAX-1 in ischemic neuronal injury have not been thoroughly elucidated. In this study, the expression and roles of HAX-1 after ischemic stress were investigated using in vivo and in vitro models.
View Article and Find Full Text PDFHAX-1 overexpression in gastric cancer promotes cell proliferation.
Transl Cancer Res
April 2020
Department of Oncology, Affiliated Hospital of Nantong University, Nantong 226001, China.
Background: HAX-1 is involved in the regulation of cellular processes such as apoptosis, proliferation and migration and is closely related to tumorigenesis and tumor metastasis. However, expression of HAX-1 in gastric cancer and its role in tumor development and progression remain unclear.
Methods: Quantitative polymerase chain reaction was used to detect the expression of HAX-1 mRNA in gastric cancer tissues and adjacent non-tumorous tissues.
miR-125b regulates the drug-resistance of breast cancer cells to doxorubicin by targeting HAX-1.
Oncol Lett
February 2018
Department of Breast Surgery, Shaoxing Shangyu People's Hospital, Shaoxing, Zhejiang 312300, P.R. China.
MircroRNAs (miRNAs) are considered as essential regulators in the tumorigenesis and chemoresistance of multiple cancer types. In the present study, it was demonstrated that the expression levels of miR-125b were significantly downregulated in the tissues of patients with breast cancer (BC), as well as the BC cell lines . To study the association between chemoresistance and miR-125b in BC, doxorubicin (DOX)-resistant MCF-7 (MCF-7/R) cells were established, and gain- and loss-of-function experiments were performed.
View Article and Find Full Text PDFChemoresistance is associated with overexpression of HAX-1, inhibition of which resensitizes drug-resistant breast cancer cells to chemotherapy.
Tumour Biol
March 2017
1 Department of Geriatrics, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Acquired resistance to standard chemotherapy is the common and critical limitation for cancer therapy. Hematopoietic cell-specific protein 1-associated protein X-1 (HAX-1) has been reported to be upregulated in numerous cancers. However, the role of HAX-1 in oncotherapy remains unclear.
View Article and Find Full Text PDFMitochondrial Omi/HtrA2 Promotes Caspase Activation Through Cleavage of HAX-1 in Aging Heart.
Rejuvenation Res
June 2017
1 Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China .
Mitochondrial homeostasis is a key process involved in cellular destiny and organic function. When mitochondrial status is abnormal, it will become a "death motor." Impaired mitochondria lead to the release of cytochrome c, and then trigger mitochondria-induced caspase activation.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!