XIAOQI WU^1,2,#, YECHUAN HE^1,2,#, YEQIN YUAN⁴, XIAN TAN^1,2, LIN ZHU^1,2, DANLING WANG^1,2,4, BINYUAN JIANG^3,4,*

BIOCELL, Vol.48, No.5, pp. 861-872, 2024, DOI:10.32604/biocell.2024.048758

Abstract Background: Nasopharyngeal carcinoma (NPC) exhibits a significant prevalence in the southern regions of China, and paclitaxel (PTX) is frequently employed as a medication for managing advanced NPC. However, drug resistance is typically accompanied by a poor prognosis. Exploring the synergistic potential of combining multiple chemotherapeutic agents may represent a promising avenue for optimizing treatment efficacy. Methods: This study investigated whether 3-Methyladenine (3-MA) could potentiated the effect of PTX and its potential molecular mechanism. Samples were divided into the following categories: Negative control (NC) with the solvent dimethyl sulfoxide (DMSO, 0.5% v/v), PTX (400 nM), 3-MA (4 mM), and PTX (400… More >

ARCHITTAPON NOKKEAW^1,2,3,#, PANNATHON THAMJAMRASSRI^1,2,3,#, NAPHAT CHANTARAVISOOT^1,4, PISIT TANGKIJVANICH^1,2,*, CHAIYABOOT ARIYACHET^1,2,*

Oncology Research, Vol.31, No.6, pp. 989-1005, 2023, DOI:10.32604/or.2023.030395

Abstract Hepatocellular carcinoma (HCC) is the leading cause of cancer death worldwide; nevertheless, current therapeutic options are limited or ineffective for many patients. Therefore, elucidation of molecular mechanisms in HCC biology could yield important insights for the intervention of novel therapies. Recently, various studies have reported dysregulation of long non-coding RNAs (lncRNAs) in the initiation and progression of HCC, including H19; however, the biological function of H19 in HCC remains unclear. Here, we show that knockdown of H19 disrupted HCC cell growth, impaired the G1-to-S phase transition, and promoted apoptosis, while overexpression of H19 yielded the opposite results. Screening for expression… More > Graphic Abstract

Yang Cao^*, Xu Shi^†, Yingmin Liu^‡, Ren Xu^§, Qing Ai^*

Oncology Research, Vol.27, No.1, pp. 117-124, 2019, DOI:10.3727/096504018X15213031799835

Abstract MicroRNA-338-3p (miR-338-3p) has been reported to be a tumor suppressor in multiple cancer types. However, the biological role of miR-338-3p and its underlying mechanism in multiple myeloma (MM) remain unclear. In the present study, we investigated the biological role and potential of miR-338-3p in MM. We found that miR-338-3p was significantly decreased in newly diagnosed and relapsed MM tissues and cell lines. Overexpression of miR-338-3p in MM cells significantly inhibited proliferation and promoted apoptosis, caspase 3, and caspase 8 activity. Bioinformatics algorithm analysis predicted that cyclin-dependent kinase 4 (CDK4) was a direct target of miR-338-3p, and this was experimentally verified… More >

Junfeng Lu^*, Zhongsong Zhao^†, Yanhong Ma^‡

Oncology Research, Vol.28, No.5, pp. 509-518, 2020, DOI:10.3727/096504020X15954139263808

Abstract The present study aimed to investigate the effect of miR-186 on proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) of hepatocellular carcinoma (HCC). In this work, miR-186 was downregulated in HCC tissues and cells, and low miR-186 level helped predict the occurrence of vascular invasion and poor prognosis in patients with HCC. miR-186 overexpression inhibited cell proliferation and tumor growth in nude mice, repressed migration and invasion abilities, and enhanced apoptosis in HCC cells. miR-186 also retarded progression of EMT. miR-186 directly bound to the 3 -untranslated regions of cyclin-dependent kinase 6 (CDK6) to inhibit its expression. Overexpression of CDK6 markedly… More >

MASOUMEH OGHABI^1,2, AVA SAFAROGHLI-AZAR^1,2, ATIEH POURBAGHERI-SIGAROODI^1,2, MOHAMMAD SAYYADI³, MOHSEN HAMIDPOUR¹, MOHAMMAD HOSSEIN MOHAMMADI¹, DAVOOD BASHASH^1,*

BIOCELL, Vol.44, No.2, pp. 183-192, 2020, DOI:10.32604/biocell.2020.08880

Abstract Pathogenesis of chronic myeloid leukemia (CML) has mostly been studied with regard to the oncogenic role of BCR/ABL fusion; however, recent disclosures have declared that the challenges with the treatment of CML patients would not be resolved until the role of other aberrancies is ignored. Given the involvement of cyclin-dependent kinases (CDKs) in the pathogenesis of CML, the present study aimed to investigate the effects of a multi-CDK inhibitor AT7519 on BCR/ABL-harboring CML-derived K562 cells. Our results showed that AT7519 effectively reduced the survival of K562 and induced its anti-proliferative effect through the induction of G2/M arrest due to elevated… More >