Huimin Zhang^*†, Yuhui Pang^†, Chuanbao Ma^†, Jianying Li^†, Huaquan Wang^*, Zonghong Shao^*

Oncology Research, Vol.26, No.3, pp. 421-429, 2018, DOI:10.3727/096504017X15049221237147

Abstract Resistance to bortezomib (BZ) is the major problem that largely limits its clinical application in multiple myeloma treatment. In the current study, we investigated whether ClC5, a member of the chloride channel family, is involved in this process. The MTT assay showed that BZ treatment decreased cell viability in three multiple myeloma cell lines (ARH77, U266, and SKO-007), with IC50 values of 2.83, 4.37, and 1.91 nM, respectively. Moreover, BZ increased the conversion of LC3B-I to LC3B-II and expressions of beclin-1 and ATG5, concomitantly with a decreased p62 expression. Pharmacological inhibition of autophagy with 3-MA… More >

Jinhui Wu, Dongshuang Wang

Oncology Research, Vol.25, No.6, pp. 863-871, 2017, DOI:10.3727/096504016X14772315906527

Abstract Chemotherapy is typically used to treat choriocarcinoma. However, a small proportion of this malignancy develops resistance to common chemotherapeutic drugs such as methotrexate (MTX) and floxuridine (FUDR). This study aimed to investigate the role and potential mechanisms of chloride intracellular channel protein 1 (CLIC1) in the development of chemoresistance in choriocarcinoma JeG3 cells. Two chemoresistant sublines were induced from their parental cell line JeG3 through intermittent exposure to MTX (named JeG3/MTX) or FUDR (named JeG3/FUDR). It was found that expression of CLIC1 was significantly higher in the chemoresistant sublines JeG3/MTX and JeG3/FUDR than in their… More >

Li-Zhou Fang^*, Jian-Qing Zhang^*, Ling Liu^*, Wei-Ping Fu^*, Jing-Kui Shu^*, Jia-Gang Feng^*, Xiao Liang^†

Oncology Research, Vol.25, No.5, pp. 819-829, 2017, DOI:10.3727/096504016X14772349843854

Abstract Cancer stem cells (CSCs) are responsible for tumorigenesis and recurrence, so targeting CSCs is an effective method to potentially cure cancer. BTB/POZ domain-containing protein 7 (Btbd7) has been found in various cancers, including lung cancer and liver cancer, but the role of Btbd7 in non-small cell lung cancer (NSCLC), CSC self-renewal, and chemoresistance is still unknown. Therefore, in this study we found that the ratio of tumor sphere formation and stem cell transcription factors in CD133⁺ cells was dramatically enhanced compared to parental cells, which indicated successful sorting of CD133⁺ cells from A549. Meanwhile, Btbd7 and More >

Feng Zhang^*, Hong Sun^†, Sai Zhang^†, Xin Yang^‡, Guogang Zhang^*, Tao Su^†

Oncology Research, Vol.25, No.5, pp. 709-719, 2017, DOI:10.3727/096504016X14772331883976

Abstract PER3, a circadian clock gene, plays an important role in colorectal cancer, but its action and underlying mechanism in colorectal cancer stem-like cells (CSCs) remain unclear. In this study, the colorectal CSCs were enriched in colorectal HCT-116 sphere-forming cells, expressing lower levels of stem cell markers CD133, CD44, LGR5, and SOX2 compared with HCT-116 cells. A drug-resistant strain from HCT-116 was established. Western blot and qRT-PCR analysis showed that PER3 was downregulated in colorectal CSCs and drug-resistant HCT-116. Overexpression of PER3 could strengthen 5-FU-induced inhibitory effects on colorectal CSCs, but knockdown of PER3 decreased its… 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 >