Zhiguo Wang^*†1, Zehui Fang^‡1, Runzhang Lu^†, Hongli Zhao^‡, Tiejun Gong^†, Dong Liu^†, Luojia Hong^‡, Jun Ma^†, Mei Zhang^*

Oncology Research, Vol.27, No.9, pp. 1035-1042, 2019, DOI:10.3727/096504019X15528367532612

Abstract Although arsenic trioxide (ATO) is a well-known antileukemic drug used for acute promyelocytic leukemia treatment, the development of ATO resistance is still a big challenge. We previously reported that microRNA- 204 (miR-204) was involved in the regulation of acute myeloid leukemia (AML) cell apoptosis, but its role in chemoresistance is poorly understood. In the present study, we showed that miR-204 was significantly increased in AML cells after ATO treatment. Interestingly, the increased miR-204 level that was negatively correlated with ATO induced the decrease in cell viability and baculoviral inhibition of apoptosis protein repeatcontaining 6 (BIRC6) expression. Overexpression of miR-204 potentiated… More >

Chao Jiang^*, Xueyan Liu^†, Meng Wang^*, Guoyue Lv^*, Guangyi Wang^*

Oncology Research, Vol.27, No.9, pp. 1025-1034, 2019, DOI:10.3727/096504018X15456687424096

Abstract miR-802 has been reported to be dysregulated in multiple tumors and contribute to tumor progression. However, its role in HCC was still largely unknown. The aim of this study is to investigate the function and mechanism of miR-802 in HCC progression. The results showed that miR-802 was upregulated in the peripheral blood and tumor tissue of HCC patients, and high levels of blood miR-802 predicted poor prognosis. miR-802 had no effect on the proliferation and migration of HCC cell lines. Interestingly, the levels of CD8/CD28 and regulated in development and DNA damage response 1 (REDD1) were declined along with the… More >

Lili Zhao^*, Yao Zhang^*, Jiaoxia Liu^*, Wei Yin^†, Dan Jin^‡, Dandan Wang^*, Wei Zhang^*

Oncology Research, Vol.27, No.9, pp. 1015-1023, 2019, DOI:10.3727/096504018X15247341491655

Abstract MicroRNAs (miRNAs) are short endogenous noncoding RNAs that frequently play vital roles in many cancer types. Herein we demonstrated that miR-185 was remarkably downregulated in NSCLC tissues compared with adjacent normal tissues. A lower level of miR-185 was associated with lymph node metastasis. Functional assays showed that upregulation of miR-185 inhibited the proliferation, colony formation, and invasion capacities of NSCLC cells in vitro. Furthermore, we found that miR-185 suppressed the epithelial–mesenchymal transition (EMT) process. Bioinformatics analysis and luciferase reporter gene assays revealed that Kruppellike factor 7 (KLF7) was the target of miR-185. Overexpression of miR-185 reduced the expression of KLF7… More >

Lihui Wang, Qi Li, Zhuo Ye, Baoping Qiao

Oncology Research, Vol.27, No.9, pp. 1007-1014, 2019, DOI:10.3727/096504018X15231148037228

Abstract Renal carcinoma greatly threatens human health, but the involved molecular mechanisms are far from complete understanding. As a master oncogene driving the initiation of many other cancers, ZBTB7 has not been established to be associated with renal cancer. Our data revealed that ZBTB7 is highly expressed in renal carcinoma specimens and cell lines, compared with normal cells. The silencing of ZBTB7 suppressed the proliferation and invasion of renal cancer cells. ZBTB7 overexpression rendered normal cells with higher proliferation rates and invasiveness. An animal study further confirmed the role of ZBTB7 in the growth of renal carcinoma. Moreover, miR-137 was identified… More >

Xue-Yi Yang, Ye Sheng

Oncology Research, Vol.27, No.9, pp. 997-1006, 2019, DOI:10.3727/096504018X15439207752093

Abstract Although miR-101 is involved in the development and progression of T-cell acute lymphoblastic leukemia (T-ALL), the underlying molecular mechanisms remain unclear. In this article, we report that miR-101 expression was inversely correlated with CX chemokine receptor 7 (CXCR7) level in T-ALL. Introducing miR-101 inhibited T-ALL cell proliferation and invasion in vitro and suppressed tumor growth and lung metastasis in vivo. CXCR7 was identified as a direct target of miR-101. The inhibitory effects of miR-101 were mimicked and counteracted by CXCR7 depletion and overexpression, respectively. Mechanistically, miR-101 targets CXCR7/STAT3 axis to reduce T-ALL growth and metastasis. Overall, these findings implied the… More >

Meng Wang^*1, Xin Wang^†1, Yuan Li^‡1, Qiang Xiao^§, Xiao-Hai Cui^*, Guo-Dong Xiao^*, Ji-Chang Wang^¶, Chong-Wen Xu^#, Hong Ren^*, Dapeng Liu^*

Oncology Research, Vol.27, No.9, pp. 987-995, 2019, DOI:10.3727/096504018X15424918479652

Abstract The aim of this study was to investigate the potential biological activities of nutlin-3 in the regulation of growth and proliferation of non-small cell lung cancer (NSCLC) stem cells (CSCs), which may help in sensitizing to axitinib-induced apoptosis. Nutlin-3 induction of p53 expression was used to test its role in controlling the cell division pattern and apoptosis of NSCLC cells. A549 cells and H460 cells were pretreated with nutlin-3 and then treated with either an Akt1 activator or shRNA-GSK3 , to investigate the potential role of p53 sensitization in the biological effects of axitinib. We also determined the expression levels… More >

Jian-Wei Wang, Xiao-Feng Wu, Xiao-Juan Gu, Xing-Hua Jiang

Oncology Research, Vol.27, No.9, pp. 979-986, 2019, DOI:10.3727/096504018X15336368805108

Abstract Cancer-associated fibroblasts (CAFs) play a predominant role in regulating tumor progression. Understanding how CAFs communicate with osteosarcoma is crucial for developing novel approaches for osteosarcoma therapy. Exosomes are able to transmit messages between cells. In this study, we demonstrated that CAFs transfer exosomes to osteosarcoma cells, which promotes osteosarcoma cell migration and invasion. Using a miRNA microarray analysis, we identified 13 miRNAs that are significantly increased in exosomes derived from cancer-associated fibroblasts (CAFs) and corresponding paracancer fibroblasts (PAFs). In vitro studies further validated that the levels of microRNA-1228 (miR-1228) were increased in CAFs, its secreted exosomes, and in recipient osteosarcoma… More >

Caiqi Liu^*, Ci Han^†, Jinfeng Liu^‡

Oncology Research, Vol.27, No.8, pp. 965-978, 2019, DOI:10.3727/096504019X15498329881440

Abstract Toll-like receptors (TLRs) are associated with tumor growth and immunosuppression, as well as apoptosis and immune system activation. TLRs can activate apoptosis and innate and adaptive immunity pathways, which can be pharmacologically targeted for the development of anticancer oncotherapies. Several studies and clinical trials indicate that TLR agonists are promising adjuvants or elements of novel therapies, particularly when used in conjunction with chemotherapy or radiotherapy. An increasing number of studies suggest that the activation of TLRs in various cancer types is related to oncotherapy; however, before this finding can be applied to clinical practice, additional studies are required. Research suggests… More >

Prasanna Rajagopalan^*†, Abdulrahim Hakami^*†, Mohammed Ragab^*, Ashraf Elbessoumy^*‡

Oncology Research, Vol.27, No.8, pp. 957-964, 2019, DOI:10.3727/096504019X15555428221646

Abstract Arylidene analogs are well proven for biological activities. FCY-302, a novel small molecule belonging to this class, was screened for its biological efficacy in leukemia and myeloma cells. FCY-302 selectively inhibited proliferation of cancer cells with GI50 values of 395.2 nM, 514.6 Nm, and 642.4 nM in HL-60, Jurkat, and RPMI-8226 cells, respectively. The compound also increased sub-G0 peak in the cancer cell cycle and favored apoptosis determined by annexin V assay. The compound decreased the antiapoptotic Bcl-2 levels and increased proapoptotic Bax proteins in leukemia and myeloma cell lines. FCY-302 attenuated the mitochondrial membrane-bound Na⁺ /K⁺ ATPase, Ca²⁺ ATPase,… More >

Yosuke Mitsui^*†, Nahoko Tomonobu^*, Masami Watanabe^†, Rie Kinoshita^*, I Wayan Sumardika^*‡, Chen Youyi^*, Hitoshi Murata^*, Ken-ichi Yamamoto^*, Takuya Sadahira^†, Acosta Gonzalez Herik Rodrigo^*†, Hitoshi Takamatsu^*, Kota Araki^*§, Akira Yamauchi^¶, Masahiro Yamamura^#, Hideyo Fujiwara^**, Yusuke Inoue^††, Junichiro Futami^‡‡, Ken Saito^§§, Hidekazu Iioka^§§, Eisaku Kondo^§§, Masahiro Nishibori^¶¶, Shinichi Toyooka^§, Yasuhiko Yamamoto^##, Yasutomo Nasu^†, Masakiyo Sakaguchi^*

Oncology Research, Vol.27, No.8, pp. 945-956, 2019, DOI:10.3727/096504019X15555408784978

Abstract S100A11, a member of the S100 family of proteins, is actively secreted from pancreatic ductal adenocarcinoma (PDAC) cells. However, the role of the extracellular S100A11 in PDAC progression remains unclear. In the present study, we investigated the extracellular role of S100A11 in crosstalking between PDAC cells and surrounding fibroblasts in PDAC progression. An abundant S100A11 secreted from pancreatic cancer cells stimulated neighboring fibroblasts through receptor for advanced glycation end products (RAGE) upon S100A11 binding and was followed by not only an enhanced cancer cell motility in vitro but also an increased number of the PDAC-derived circulating tumor cells (CTCs) in… More >