YIBIN RUAN¹, ZHONGMING XIE², QIONG LIU², LIXIAO ZHANG², XIKUI HAN², XIAOYAN LIAO², JIAN LIU^1,*, FENGGUANG GAO^2,*

BIOCELL, Vol.45, No.4, pp. 1059-1067, 2021, DOI:10.32604/biocell.2021.015261

Abstract Nicotine and menthol, agonists of nicotinic acetylcholine receptor (nAChR) and transient receptor potential melastatin type 8 (TRPM8), serve important roles in the prevention of cell death-involved neurodegenerative diseases. However, the potential synergistic effects of nicotine and menthol on anti-apoptotic ability are still uncertain. In the present study, the potential synergistic effects of nicotine and menthol on cisplatin or amyloid β_1-42 induced cell model of the neurodegenerative diseases were explored by assessing cell viability, TNF-α expression, caspase-3 activation, and the collapse of mitochondrial membrane potential in human SH-SY5Y neuroblastoma cells. Statistical significance was tested using Student’s t-test… More >

SUFANG ZHANG^1,2,#, XIANG LV^1,#, LI LI^3,#, YINGBIN LUO¹, HUINAN XIANG¹, LIXIN WANG^2,*, YAN LI^1,*

BIOCELL, Vol.45, No.1, pp. 167-175, 2021, DOI:10.32604/biocell.2021.013636

Abstract Chemotherapy is widely used for non-small cell lung cancer (NSCLC) patients at a late stage; however, NSCLC patients often acquire resistance to chemotherapeutic drugs, thus limiting the therapy efficacy. Melittin, a major component of bee venom, possesses anti-tumor activity in various cancer cells. Here, we examined the effects of melittin on A549/DDP cisplatin-resistant lung adenocarcinoma cells and xenografts formed from this cell line and investigated the possible target of melittin. Treatment with melittin resulted in the induction of cell apoptosis, glycolysis inhibition, and reduction of phosphorylated AKT (p-AKT) in A549/DDP cells. We also identified that… More >

Huasong Liu^*1, Jun Zhang^*1, Xiangyu Luo^*, Min Zeng^*, Liqiang Xu^*, Qunxian Zhang^*, Hua Liu^*, Jialong Guo^*, Lanlan Xu^†

Oncology Research, Vol.28, No.1, pp. 65-73, 2020, DOI:10.3727/096504019X15656904013079

Abstract Emerging evidence has demonstrated that long noncoding RNAs (lncRNAs) mediate the development of esophageal squamous cell carcinoma (ESCC) via various pathophysiological pathways. This study explored the impact of the lncRNA FOXD2-AS1 on cisplatin resistance in ESCC and its possible mechanisms. Upregulation of FOXD2-AS was detected in patients with ESCC and ESCC cells that are resistant to cisplatin. In an in vitro assay, knockdown of FOXD2-AS1 noticeably inhibited cell invasion and growth, triggered cell death, and repressed the stimulation of the Akt/mTOR axis in cisplatin-resistant ESCC cells (TE-1/DDP). Conversely, the overexpression of FOXD2-AS1 remarkably increased cell More >

Xiaohui Shen, Xia Gao, Hui Li, Yajun Gu, Junguo Wang

Oncology Research, Vol.27, No.1, pp. 73-80, 2019, DOI:10.3727/096504018X15201099883047

Abstract Laryngeal carcinoma is a type of head and neck carcinoma with a high incidence and mortality. Chemotherapy treatments of human laryngeal carcinoma may fail due to the development of chemoresistance. Tissue inhibitor of metalloproteinase 3 (TIMP-3) has been shown to be implicated in a number of pathological processes typical for cancer. The present study aims to investigate the involvement of TIMP-3 in the chemoresistance of laryngeal carcinoma. We showed that TIMP-3 expression was significantly decreased in chemoresistant laryngeal carcinoma tissues compared with chemosensitivity tissues. Patients with low TIMP-3 expression exhibited poorer overall survival than those… More >

Entsar A. SAAD¹, Reda S. EL-DEMERDASH², Eman M. ABD EI-FATTAH¹

BIOCELL, Vol.43, No.2, pp. 73-80, 2019, DOI:10.32604/biocell.2019.07020

Abstract Cisplatin is a powerful anticancer drug but its nephrotoxic effects limit its clinical use. We aimed to evaluate the effect of mesenchymal stem cells (MSCs) injection or of captopril to counteract the cisplatin-induction of nephropathy. MSCs isolation, preparation and tracking, transforming growth factor-β (TGF-β) and interleukin-10 (IL-10) expressions, kidney function tests, oxidative stress state, and histological examinations were done. Cisplatininduced nephropathy was indicated biochemically and confirmed histopathologically. MSCs treatment showed normal kidney architecture, and significantly decreased oxidative stress and TGF-β while increased IL-10 and improved kidney function tests. Rats treated with cisplatin + captopril More >

Farui Sun^*, Yuanjin Zhang^*, Lijun Xu^*, Songbai Li^*, Xiang Chen^*, Ling Zhang^*, Yifan Wu^†, Jun Li^*

Oncology Research, Vol.26, No.4, pp. 655-664, 2018, DOI:10.3727/096504017X15119525209765

Abstract Although cisplatin has been shown to be an integral part of chemotherapy regimen in osteosarcoma (OS) treatment, toxicity issues and chemoresistance have hindered therapeutic development for OS. Exploring novel combination therapy methods is needed to circumvent the limitations of cisplatin alone. The proteasome inhibitor MG132 has shown antitumor effects in many solid tumors. However, little is known about its effects in combination with cisplatin in OS cells. In this study, we examined the effects of MG132 in combination with cisplatin in human OS cells (MG-63 and HOS). MG132 and cisplatin were applied to OS cells,… More >

Anne Riemann^*, Antje Güttler^†, Verena Haupt^*, Henri Wichmann^†, Sarah Reime^*, Matthias Bache^†, Dirk Vordermark^†, Oliver Thews^*

Oncology Research, Vol.26, No.2, pp. 191-200, 2018, DOI:10.3727/096504017X14965111926391

Abstract Carbonic anhydrase (CA) IX has emerged as a promising target for cancer therapy. It is highly upregulated in hypoxic regions and mediates pH regulation critical for tumor cell survival as well as extracellular acidification of the tumor microenvironment, which promotes tumor aggressiveness via various mechanisms, such as augmenting metastatic potential. Therefore, the aim of this study was to analyze the complex interdependency between CA IX and the tumor microenvironment in prostate tumor cells with regard to potential therapeutic implications. CA IX was upregulated by hypoxia as well as acidosis in prostate cancer cells. This induction… More >

Xin Jin^*, Shenghua Tian^†, Pingping Li^‡

Oncology Research, Vol.25, No.6, pp. 939-946, 2017, DOI:10.3727/096504016X14809827856524

Abstract Hepatocellular carcinoma (HCC) is one of the most common malignant diseases in the world. Mutations, overexpression, and improper recruitment of HATs can lead to tumorigenesis. HAT1 is the first histone acetyltransferase identified and is related with developing HCC, but the mechanism is still unclear. Interestingly, we found that HAT1 was upregulated in HCC patient specimens and showed that its upregulation facilitates HCC cell growth in vitro and in vivo. Moreover, we demonstrated that HAT1 promoted glycolysis in HCC cells and knockdown of HAT1 sensitized HCC cells to apoptotic death induced by cisplatin. Our results suggest More >

Tao Xie^*, Yao Li^†, Shi-Lei Li^*, Hai-Feng Luo^‡

Oncology Research, Vol.24, No.6, pp. 447-453, 2016, DOI:10.3727/096504016X14685034103590

Abstract Although astragaloside IV exhibits anti-inflammation, immunoregulatory, and anticancer properties, the chemosensitization effects of astragaloside IV in colorectal cancer have never been reported. Our study tested whether astragaloside could increase cisplatin sensitivity in colorectal cancer. CCK-8 assay was used to measure the cell viability of colorectal cancer cells. Quantitative real-time PCR and Western blot were performed to determine the mRNA and protein expression, respectively. Our data revealed that astragaloside IV administration significantly suppressed the cell growth of colorectal cancer cells, whereas no obvious cytotoxicity of astragaloside IV was observed in nonmalignant colonic cells. In addition, combined… More >

Sheng Li, Zhengli Cui, Xianfeng Meng

Oncology Research, Vol.24, No.4, pp. 279-286, 2016, DOI:10.3727/096504016X14666990347554

Abstract Poly(ADP-ribose) polymerase 1 (PARP-1) is reported to be involved in DNA repair and is now recognized as a key regulator in carcinogenesis. However, the potential role and the molecular mechanism underlying the effect of PARP-1 on osteosarcoma (OS) cells have not been elucidated. In this study, the results showed that knockdown of PARP-1 resulted in decreased cell proliferation, increased cell apoptosis, and G₀/G₁ phase arrest in U2OS cells. In addition, increased expression of active caspase 3 and Bax, but reduced Bcl-2, cyclin D1, and phosphorylated extracellular signal regulated kinase 1/2 (pERK1/2) were observed in PARP-1 knockdown More >