Oncology Research Editorial Office

Oncology Research, Vol.32, No.8, pp. 1379-1379, 2024, DOI:10.32604/or.2024.055034 - 17 July 2024

Abstract This article has no abstract. More >

WEI SHI^1,2,3,#, JIANXIA LIN^1,2,3,#, RONG JIN^1,2,3, XIANJING XIE^1,2,3, YAN LIANG^1,2,3,*

BIOCELL, Vol.47, No.4, pp. 869-877, 2023, DOI:10.32604/biocell.2023.026037 - 08 March 2023

Abstract Background: LncRNA DLX6-AS1 has been uncovered to exert effects on various cancers. Nevertheless, the impacts of DLX6-AS1 on endometrial cancer (EC) development remained obscure. The study explored the influence of DLX6-AS1 on EC progression via the microRNA (miR)-374a-3p/zinc-finger protein (ZFX) axis.Methods: EC cell lines were collected and DLX6-AS1, miR-374a-3p, and ZFX levels in EC cell lines were detected. The EC cells were transfected with DLX6-AS1, miR-374a-3p, and ZFX constructs to examine the biological functions of EC cells. The xenograft model was established for detecting tumor growth. Rescue experiments were conducted to verify the interaction of DLX6-AS1, More > Graphic Abstract

YUANNA DU^1,#, WENWEN GONG^2,#, JING LIANG^1,#, RUKUN ZANG¹, JUNJUN MOU¹

BIOCELL, Vol.46, No.5, pp. 1181-1188, 2022, DOI:10.32604/biocell.2022.016148 - 06 January 2022

Abstract Endometrial cancer remains to be a major type of malignancy in threatening female life. Molecular insights in advancing our understanding of endometrial tumorigenesis are much needed. We here report that a less-studied protein Dihydropyrimidinase like 3 (DPYSL3) is a potent tumor suppressor. DPYSL3 is uniquely regulated by wild type p53 (wtp53), and its expression is at the highest level when cells carry wtp53 and are exposed to hypoxia. We reveal that wtp53 can bind DPYSL3 promoter to enhance DPYSL3 expression and in turn, the elevated DPYSL3 can restrain cancer cell proliferation and invasion in vitro and in… More >

Jinfeng Qu^*, Lei Zhang^†, Lanyu Li^*, Yujie Su^*

Oncology Research, Vol.27, No.1, pp. 81-88, 2019, DOI:10.3727/096504018X15202988139874

Abstract This study investigated the tumor-suppressive role of miR-148b in regulating endoplasmic reticulum metalloprotease 1 (ERMP1) expression and the oxidative stress response in endometrial cancer cells. Human endometrial cancer RL95-2 cells were used and transfected with miR-148b mimic, miR-148b inhibitor, or their scrambled negative control. Thereafter, the transfection efficiency was determined by RT-qPCR, and cell proliferation was assessed by MTT assay. The dual-luciferase reporter assay, Western blot, and RT-qPCR were conducted to determine the target gene of miR-148b. ERMP1 is a putative target of miR-148b, and thereby the overexpression and downregulation of ERMP1 on the proliferation… More >

Pedro Fong^*1, Cheng N. Ao^*†1, Kai I. Tou^*, Ka M. Huang^*, Chi C. Cheong^*, Li R. Meng^*

Oncology Research, Vol.27, No.2, pp. 237-251, 2019, DOI:10.3727/096504018X15235274183790

Abstract The aim of this study was to investigate the inhibition effects of cordycepin and its derivatives on endometrial cancer cell growth. Cytotoxicity MTT assays, clonogenic assays, and flow cytometry were used to observe the effects on apoptosis and regulation of the cell cycle of Ishikawa cells under various concentrations of cordycepin, cisplatin, and combinations of the two. Validated in silico docking simulations were performed on 31 cordycepin derivatives against adenosine deaminase (ADA) to predict their binding affinities and hence their potential tendency to be metabolized by ADA. Cordycepin has a significant dose-dependent inhibitory effect on More >

Haizhen Wang^*, Zhenghua Tang^*, Ting Li^*, Menglu Liu^*, Yong Li^†, Baoling Xing^*

Oncology Research, Vol.27, No.9, pp. 1051-1060, 2019, DOI:10.3727/096504019X15561873320465

Abstract Medroxyprogesterone (MPA) is used for the conservative treatment of endometrial cancer. Unfortunately, progesterone resistance seriously affects its therapeutic effect. The purpose of the current study was to investigate the influence of deletion of AT-rich interactive domain 1A (ARID1A) in progesterone resistance in Ishikawa cells. Ablation of ARID1A was conducted through the CRISPR/Cas9 technology. Acquired progesterone-resistant Ishikawa (Ishikawa-PR) cells were generated by chronic exposure of Ishikawa cells to MPA. The sensitivity of the parental Ishikawa, Ishikawa-PR, and ARID1A-deficient cells to MPA and/or LY294002 was determined using the Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis.… More >