RUOYU CHEN¹, YIMAN WU¹, FENG WANG¹, JUNTAO ZHOU¹, HUAZHANG ZHUANG¹, WEI LI^2,*

BIOCELL, Vol.48, No.7, pp. 1037-1046, 2024, DOI:10.32604/biocell.2024.051074 - 03 July 2024

Abstract Background: Oleanolic acid (OA), a pentacyclic triterpenoid exhibiting specific anti-cancer properties and highly effective antioxidant activity, was isolated from traditional Chinese medicinal herbs. Conversely, the OA that impacts colon cancer (CC) cells and its underlying mechanisms remain poorly understood. Methods: The cytotoxic effect of OA alone or OA-5-Fluorouracil (5-FU) combination on normal and CC cells was analyzed by methyl thiazolyl diphenyl-tetrazolium bromide (MTT). Then, the impact of OA on CC cell lines (LoVo and HT-29) proliferation and stemness were measured using colon formation and tumorsphere formation assays. Octamer-binding transcription factor 4 (Oct4), Prominin-1 (CD133), Nanog,… More >

YONGKANG SHI, JUN MA, KE CHEN, BIN CHEN^*

Oncology Research, Vol.30, No.4, pp. 201-210, 2022, DOI:10.32604/or.2022.027584 - 31 January 2023

Abstract 5-Fluorouracil (5-FU) is a commonly used chemotherapeutic agent for various cancers. However, the drug resistance developed by tumor cells hinders the therapeutic effect. Konjac glucomannan (KGM) is indicated to sensitize 5-FU-resistant hepatocellular carcinoma (HCC) cells to 5-FU. In our study, we found that KGM or 5-FU treatment alone did not affect the malignant cell behaviors and endoplasmic reticulum (ER) stress of 5-FU-resistant HCC cells or HepG2/5-FU and Bel-7402/5-FU cells, while cotreatment with KGM and 5-FU significantly facilitated HCC cell apoptosis and ER stress and suppressed cell proliferation potential and migration abilities. Moreover, we explored the… More >

Jianing Yi^*, Shuai Chen^*, Pingyong Yi^†, Jinlin Luo^*, Meng Fang^*, Yang Du^*, Lianhong Zou^*, Peizhi Fan^*

Oncology Research, Vol.28, No.5, pp. 519-831, 2020, DOI:10.3727/096504020X15960154585410

Abstract 5-Fluorouracil (5-FU) is a widely used chemotherapeutic agent for breast cancer. However, acquired chemoresistance leads to a loss of its efficacy; methods to reverse are urgently needed. Some studies have shown that pyrotinib, an ErbB receptor tyrosine kinase inhibitor, is effective against HER2+ breast cancer. However, whether pyrotinib sensitizes 5-FU-resistant breast cancer cells to 5-FU is unknown. We hypothesized that the combination of pyrotinib and 5-FU would show synergistic antitumor activity, and pyrotinib could reverse 5-FU resistance in HER2+ breast cancer cells in vitro and in vivo. Our data showed that pyrotinib inhibited the growth… More >

Jianjun Shen^*1, Weina Niu^†1, Hongbo Zhang^*, Ma Jun^*, Hongyan Zhang^*

Oncology Research, Vol.28, No.9, pp. 961-963, 2020, DOI:10.3727/096504022X16414984936746

Abstract Gastric cancer is the fourth most common malignancy and the third leading cause of cancer-related deaths worldwide. This study aimed to investigate the expression patterns, biological roles, and underlying mechanisms of microRNA-147 (miR-147) in gastric cancer. The present study demonstrated that miR-147 was significantly upregulated in gastric cancer tissues and cell lines. Downregulation of miR-147 decreased cell proliferation and enhanced the chemosensitivity of gastric cancer cells to 5-fluorouracil (5-FU) through the cell apoptosis pathway. In addition, phosphatase and tensin homolog (PTEN) was mechanically identified as the direct target of miR-147 in gastric cancer. PTEN knockdown More >

Lihua Jiang^*1, Wenchuan Yang^*1, Weishi Bian^†, Hailin Yang^*, Xia Wu^*, Yuhua Li^*, Wen Feng^*, Xuejian Liu^*

Oncology Research, Vol.27, No.1, pp. 19-27, 2019, DOI:10.3727/096504018X15193469240508

Abstract The dysregulation of microRNAs (miRNAs) plays an important function in the onset and progression of gastric cancer (GC). In addition, aberrantly expressed miRNAs affect the chemosensitivity of GC cells to chemotherapeutic drugs. Hence, miRNA-based targeted therapy might be applied to treat patients with GC exhibiting chemotherapeutic resistance. In this study, miRNA-623 (miR-623) expression was downregulated in GC tissues and cell lines. Functional analysis showed that the restored miR-623 expression could inhibit the proliferation of GC cells and enhance their chemosensitivity to 5-FU via the cell apoptosis pathway. Cyclin D1 (CCND1) was identified as a direct More >

Qiuying Quan^*1, Fengyun Zhong^†1, Xinwei Wang^‡, Kai Chen^§, Lingchuan Guo^*

Oncology Research, Vol.27, No.7, pp. 779-788, 2019, DOI:10.3727/096504018X15442985680348

Abstract The aim of this study was to investigate the underlying mechanisms that transforming growth factor- (TGF- )-mediated epithelial-to-mesenchymal transition (EMT) in tumor cells contributes to 5-FU resistance. A series of experiments involving cell viability and caspase activity analyses, siRNA transfection, RNA isolation, and quantitative-PCR (qPCR) assay, cell migration analysis, Western blotting analysis of total protein and membrane protein were performed in this study. Mouse xenograft model was used to determine the effect of the PAR2 inhibitor in vivo. In this study, we found that protease-activated receptor 2 (PAR2) induction in 5-FU therapy is correlated with… More >

Jianjun Shen^*1, Weina Niu^†1, Hongbo Zhang^*, Ma Jun^*, Hongyan Zhang^*

Oncology Research, Vol.26, No.6, pp. 901-911, 2018, DOI:10.3727/096504017X15061902533715

Abstract Gastric cancer is the fourth most common malignancy and the third leading cause of cancer-related deaths worldwide. This study aimed to investigate the expression patterns, biological roles, and underlying mechanisms of microRNA-147 (miR-147) in gastric cancer. The present study demonstrated that miR-147 was significantly upregulated in gastric cancer tissues and cell lines. Downregulation of miR-147 decreased cell proliferation and enhanced the chemosensitivity of gastric cancer cells to 5-fluorouracil (5-FU) through the cell apoptosis pathway. In addition, phosphatase and tensin homolog (PTEN) was mechanically identified as the direct target of miR-147 in gastric cancer. PTEN knockdown More >

Enrico Mini^*, Ida Landini^*, Laura Lucarini^†, Andrea Lapucci^*, Cristina Napoli^‡, Gabriele Perrone^*, Renato Tassi^*, Emanuela Masini^†, Flavio Moroni^†, Stefania Nobili^‡

Oncology Research, Vol.26, No.2, pp. 333-334, 2018, DOI:10.3727/096504018X15187172557369

Abstract The poly(ADP-ribose) polymerase (PARP) enzymes play a key role in the regulation of cellular processes (e.g., DNA damage repair, genomic stability). It has been shown that PARP inhibitors (PARPIs) are selectively cytotoxic against cells having dysfunctions in genes involved in DNA repair mechanisms (synthetic lethality). Drug-induced PARP inhibition potentiates the activity of anticancer drugs such as 5-fluorouracil in enhancing DNA damage, whose repair involves PARP-1 activity. The aim of this study was to evaluate the inhibitory effects of a novel PARPI, HYDAMTIQ, on growth in human tumor cell lines characterized by different features with regard… More >

Enrico Mini^*, Ida Landini^*, Laura Lucarini^†, Andrea Lapucci^*, Cristina Napoli^‡, Gabriele Perrone^*, Renato Tassi^*, Emanuela Masini^†, Flavio Moroni^†, Stefania Nobili^‡

Oncology Research, Vol.25, No.9, pp. 1441-1451, 2017, DOI:10.3727/096504017X14926854178616

Abstract The poly(ADP-ribose) polymerase (PARP) enzymes play a key role in the regulation of cellular processes (e.g., DNA damage repair, genomic stability). It has been shown that PARP inhibitors (PARPIs) are selectively cytotoxic against cells having dysfunctions in genes involved in DNA repair mechanisms (synthetic lethality). Drug-induced PARP inhibition potentiates the activity of anticancer drugs such as 5-fluorouracil in enhancing DNA damage, whose repair involves PARP-1 activity. The aim of this study was to evaluate the inhibitory effects of a novel PARPI, HYDAMTIQ, on growth in human tumor cell lines characterized by different features with regard… More >

Makoto Akiyama^*†, Yoshihiro Sowa^*, Tomoyuki Taniguchi^*, Motoki Watanabe^*, Shingo Yogosawa^‡, Jo Kitawaki^†,Toshiyuki Sakai^*

Oncology Research, Vol.25, No.8, pp. 1245-1252, 2017, DOI:10.3727/096504017X14850164661097

Abstract Ovarian cancer is the most lethal disease among gynecological malignancies. More effective therapy is required to counter high recurrence rates and chemotherapy resistance. We investigated the efficacy and molecular mechanisms of three combined treatments (TCTs)—a novel histone deacetylase (HDAC) inhibitor OBP-801/YM753, 5-fluorouracil (5-FU), and paclitaxel (PTX)—in human ovarian cancer SKOV-3 and OVCAR-3 cells. The inhibition of cell growth was stronger with TCTs than with each single agent and with two combined treatments. The TCTs significantly induce G₂ phase arrest in both cell lines. We then analyzed the molecular mechanisms and found that the TCTs increased the More >