Huihui Shi^1,#, Lei Chen^2,#, Juan Huang^3,#, Xuejing Lin², Lei Huang⁴, Min Tang⁴, Kai Lu^5,*, Wenchao Wang^4,*, Maoling Zhu^1,§,*

Oncology Research, Vol.34, No.1, 2026, DOI:10.32604/or.2025.068737 - 30 December 2025

Abstract Background: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related mortality worldwide. This study aimed to identify key genes involved in HCC development and elucidate their molecular mechanisms, with a particular focus on mitochondrial function and apoptosis. Methods: Differential expression analyses were performed across three datasets—The Cancer Genome Atlas (TCGA)-Liver Hepatocellular Carcinoma (LIHC), GSE36076, and GSE95698—to identify overlapping differentially expressed genes (DEGs). A prognostic risk model was then constructed. Cysteine/serine-rich nuclear protein 1 (CSRNP1) expression levels in HCC cell lines were assessed via western blot (WB) and quantitative reverse transcription polymerase chain reaction (qRT-PCR).… More > Graphic Abstract

Yi-Tzu Chen^1,2,3,#, Shao-Hsuan Kao^4,5,#, Chun-Yi Chuang^6,7, Chun-Wen Su^4,5, Wei-En Yang^4,5, Chih-Hsin Tang^8,9,10, Shun-Fa Yang^4,5,*, Chiao-Wen Lin^2,3,*

Oncology Research, Vol.33, No.11, pp. 3387-3404, 2025, DOI:10.32604/or.2025.069877 - 22 October 2025

Abstract Background: Alisol A is a natural compound isolated from Alismatis Rhizoma, known for its diverse pharmacological activities, including anticancer and neuroprotective effects. This study aimed to explore the anticancer effects of Alisol A on oral cancer cells and elucidate its underlying mechanisms. Methods: Cell viability was measured by MTT assay, cell cycle by flow cytometry, and apoptosis by Annexin V/PI staining and caspase activation. Regulation of signaling pathways was analyzed using an apoptosis-related protein array, immunoblotting, and specific kinase inhibitors. Results: Alisol A reduced the viability of oral cancer cell lines, induced sub-G1 phase accumulation, and augmented… More >

PINGHUA TU, SHANSHAN WANG, KELAN DENG, XINJUN LI, ZHANLING WU^*

BIOCELL, Vol.48, No.11, pp. 1603-1612, 2024, DOI:10.32604/biocell.2024.054364 - 07 November 2024

Abstract Objectives: The antitumor effects of pyropheophorbide-α methyl ester-mediated photodynamic therapy (MPPa-PDT) were observed in several cancers. The objective of this investigation was to examine the antineoplastic efficacy of MPPa-PDT acting on lung carcinoma A549 cells and further elaborate mechanisms. Methods: The viability of A549 cells was examined with cell counting kit-8 after MPPa-PDT disposal. Hoechst 33342 staining, monodansylcadaverine (MDC) staining, and transmission electron microscopy were employed to observe apoptotic bodies and autophagic vesicles. Flow cytometry with Annexin V/propidium iodide (PI) labeling objectively assessed cell death. The expression of associated proteins, including Caspase-3, Beclin-1, LC-3II, and More > Graphic Abstract

Oncology Research Editorial Office

Oncology Research, Vol.32, No.9, pp. 1523-1523, 2024, DOI:10.32604/or.2024.056118 - 23 August 2024

Abstract This article has no abstract. More >

Xiaowen Chen^*1, Jianli Chen^†1

Oncology Research, Vol.26, No.3, pp. 363-372, 2018, DOI:10.3727/096504017X14953948675421

Abstract This study intended to investigate the effects of miR-3188 on breast cancer and to reveal the possible molecular mechanisms. miR-3188 was upregulated and TUSC5 was downregulated in breast cancer tissues and MCF-7 cells compared to normal tissue and MCF-10 cells. After MCF-7 cells were transfected with miR-3188 inhibitor, cell proliferation and migration were inhibited, whereas apoptosis was promoted. Luciferase reporter assay suggested that TUSC5 was a target gene of miR-3188. In addition, miR-3188 overexpression increased the p-p38 expression, while miR-3188 suppression decreased the p-p38 expression significantly. miR-3188 regulated breast cancer progression via the p38 MAPK More >

Maitham A. Khajah, Princy M. Mathew, Yunus A. Luqmani

Oncology Research, Vol.25, No.8, pp. 1283-1295, 2017, DOI:10.3727/096504017X14883245308282

Abstract Current mainstream pharmacological options for the treatment of endocrine-resistant breast cancer have limitations in terms of their side effect profile and lack of discrimination between normal and cancer cells. In the current study, we assessed the responses of normal breast epithelial cells MCF10A, estrogen receptorpositive (ER+ ) MCF-7, and ER-silenced pII breast cancer cells to inhibitors (either individually or in combination) of downstream signaling molecules. The expression/activity of ERK1/2, p38 MAPK, and Akt was determined by Western blotting. Cell proliferation, motility, and invasion were determined using MTT, wound healing, and Matrigel assays, respectively. Morphological changes… More >