CXCL3 overexpression promotes the tumorigenic potential of uterine cervical cancer cells via the MAPK/ERK pathway

2019 ◽  
Vol 235 (5) ◽  
pp. 4756-4765 ◽  
Author(s):  
Ya‐Ling Qi ◽  
Yue Li ◽  
Xia‐Xia Man ◽  
Hong‐Yu Sui ◽  
Xiao‐Lian Zhao ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Uterine Cervical Cancer ◽  
Erk Pathway ◽  
Tumorigenic Potential ◽  
Cervical Cancer Cells

scholarly journals The Application of Arsenic Trioxide in Ameliorating ABT-737 Target Therapy on Uterine Cervical Cancer Cells through Unique Pathways in Cell Death

Cancers ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 108 ◽  
Author(s):  
I-Lun Hsin ◽  
Ying-Hsiang Chou ◽  
Wei-Li Hung ◽  
Jiunn-Liang Ko ◽  
Po-Hui Wang
Keyword(s):  
Cervical Cancer ◽  
Synergistic Effect ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Combination Treatment ◽  
Combined Treatment ◽  
B Cell Lymphoma ◽  
Uterine Cervical Cancer ◽  
Cervical Cancer Cells ◽  
Mediated Reduction

ABT-737, a B cell lymphoma-2 (Bcl-2) family inhibitor, activates apoptosis in cancer cells. Arsenic trioxide is an apoptosis activator that impairs cancer cell survival. The aim of this study was to evaluate the effect of a combination treatment with ABT-737 and arsenic trioxide on uterine cervical cancer cells. MTT (3-(4,5-dimethylthiazol-2-yl)-25-diphenyltetrazolium bromide) assay revealed that ABT-737 and arsenic trioxide induced a synergistic effect on uterine cervical cancer cells. Arsenic trioxide enhanced ABT-737-induced apoptosis and caspase-7 activation and the ABT-737-mediated reduction of anti-apoptotic protein Mcl-1 in Caski cells. Western blot assay revealed that arsenic trioxide promoted the ABT-737-mediated reduction of CDK6 and thymidylate synthetase in Caski cells. Arsenic trioxide promoted ABT-737-inhibited mitochondrial membrane potential and ABT-737-inhibited ANT expression in Caski cells. However, ABT-737-elicited reactive oxygen species were not enhanced by arsenic trioxide. The combined treatment induced an anti-apoptosis autophagy in SiHa cells. This study is the first to demonstrate that a combination treatment with ABT-737 and arsenic trioxide induces a synergistic effect on uterine cervical cancer cells through apoptosis. Our findings provide new insights into uterine cervical cancer treatment.

scholarly journals TM7SF2 regulates cell proliferation and apoptosis by activation of C-Raf/ERK pathway in cervical cancer

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yichi Xu ◽  
Xin Chen ◽  
Shuya Pan ◽  
Zhi-wei Wang ◽  
Xueqiong Zhu
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cholesterol Metabolism ◽  
Vital Role ◽  
Erk Pathway ◽  
Tumorigenesis And Progression ◽  
Cervical Cancer Cells ◽  
Cancer Tissues

AbstractTransmembrane 7 superfamily member 2 (TM7SF2) coding an enzyme involved in cholesterol metabolism has been found to be differentially expressed in kinds of tissues. Nevertheless, the role of TM7SF2 in the regulation of growth and progression among various cancers is unclear. In this study, the immunohistochemistry (IHC) assay, real-time RT-PCR and western blotting analysis were used to determine the TM7SF2 expression in cervical cancer tissues. Next, we used multiple methods to determine the ability of cell proliferation, migration, invasion, apoptosis, and cell cycle in cervical cancer cells after TM7SF2 modulation, such as CCK8 assay, colony formation assay, Transwell assay, wound healing assay, and flow cytometry. Our results revealed that upregulation of TM7SF2 facilitated cell proliferation and metastasis, suppressed cell apoptosis and prevented G0/G1 phase arrests in C33A and SiHa cells. Consistently, the opposite effects were observed after TM7SF2 knockout in cervical cancer cells. Further, we found that TM7SF2 participated in promoting tumorigenesis and progression via activation of C-Raf/ERK pathway in cervical cancer, which can be partly reversed by Raf inhibitor LY3009120. Moreover, TM7SF2 overexpression contributed to enhancement of xenograft tumor growth in vivo. Our findings indicated that TM7SF2 plays a vital role in tumor promotion by involving in C-Raf/ERK activation. Therefore, TM7SF2 could serve as a therapeutic target in future cervical cancer treatment.

scholarly journals Effects of ABT‑737 combined with irradiation treatment on uterine cervical cancer cells

2019 ◽  
Author(s):  
Huang‑Pin Shen ◽  
Wen‑Jun Wu ◽  
Jiunn‑Liang Ko ◽  
Tzu‑Fan Wu ◽  
Shun‑Fa Yang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Uterine Cervical Cancer ◽  
Irradiation Treatment ◽  
Cervical Cancer Cells

scholarly journals Abnormal level of paxillin in cervical cancer cells is involved in tumor progression and invasion

2021 ◽  
Author(s):  
Hongqing Gu ◽  
Jing Wen
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Uterine Cervical Cancer ◽  
Cancer Growth ◽  
Over Expression ◽  
Apoptosis Inhibition ◽  
Cervical Cancer Cells ◽  
Elevated Expression ◽  
Abnormal Level

Human papillomavirus (HPV) is the primary causative agent for the uterine cervical cancer. The expression of oncoproteins E6/E7 promotes apoptosis inhibition and increases the risk of cervical cancer progression. Some research reported that elevated expression of paxillin (PXN) stimulated cancer growth and invasion. However, the clinical significance of PXN in cervical cancer has not been well characterized so far. We found that PXN mRNA expression and protein level are significantly upregulated in cervical cancer cells compared to adjacent normal cells. Furthermore, the paxillin over-expression was correlated with potential of tumorigenesis and invasion. Cervical cancer cells with increased paxillin expression had an ability to form more tumor clones and were characterized by higher invasiveness as well. Therefore, our findings suggest that paxillin may act as an important prognostic factor for cervical cancer patients as it promotes tumor regeneration and invasion.

scholarly journals O‐GlcNAcylation Affects the Tumorigenic Potential of Cervical Cancer Cells

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Nicole Jaskiewicz ◽  
Stephanie Parisi ◽  
Crystal Hermawan ◽  
David Townson
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Tumorigenic Potential ◽  
Cervical Cancer Cells

Enhanced Expression of Thymidylate Synthase Mediates Resistance of Uterine Cervical Cancer Cells to Radiation

Oncology ◽  
2002 ◽  
Vol 63 (2) ◽  
pp. 185-191 ◽  
Author(s):  
Yasushi Saga ◽  
Mitsuaki Suzuki ◽  
Hiroaki Mizukami ◽  
Masashi Urabe ◽  
Masakazu Fukushima ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Thymidylate Synthase ◽  
Uterine Cervical Cancer ◽  
Cervical Cancer Cells ◽  
Enhanced Expression
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