Juan Gu^*, Chang-fu Cui^†, Li Yang^‡, Ling Wang^*, Xue-hua Jiang^*

Oncology Research, Vol.28, No.6, pp. 681-682, 2020, DOI:10.3727/096504021X16137463165424

Abstract Colon cancer (CC) is the third most common cancer worldwide. Emodin is an anthraquinone-active substance that has the ability to affect tumor progression. Our study aims to explore the effects and the relevant mechanism of emodin on the invasion and migration of CC in vitro and in vivo. In our study, we found that emodin inhibited the invasion and migration abilities of RKO cells and decreased the expression of matrix metalloproteinase-7 (MMP-7), MMP-9, and vascular endothelial growth factor (VEGF) in a dose-dependent manner. Further research suggested that emodin inhibited EMT by increasing the mRNA level of E-cadherin and decreasing the… More >

WM Farhan Syafiq B. WM Nor^*†, Ivy Chung^‡§, Nur Akmarina B. M. Said^†

Oncology Research, Vol.28, No.6, pp. 615-629, 2020, DOI:10.3727/096504020X16037933185170

Abstract Breast cancer is the most commonly diagnosed cancer among women and one of the leading causes of cancer mortality worldwide, in which the most severe form happens when it metastasizes to other regions of the body. Metastasis is responsible for most treatment failures in advanced breast cancer. Epithelial–mesenchymal transition (EMT) plays a significant role in promoting metastatic processes in breast cancer. MicroRNAs (miRNAs) are highly conserved endogenous short noncoding RNAs that play a role in regulating a broad range of biological processes, including cancer initiation and development, by functioning as tumor promoters or tumor suppressors. Expression of miR-548m has been… More >

Weili Min^*1, Liangzhang Sun^†1, Burong Li^‡, Xiao Gao^*, Shuqun Zhang^*, Yang Zhao^*

Oncology Research, Vol.28, No.9, pp. 857-872, 2020, DOI:10.3727/096504021X16203818567367

Abstract EMT confers increased metastatic potential and the resistance to chemotherapies to cancer cells. However, the precise mechanisms of EMT-related chemotherapy resistance remain unclear. c-Src-mediated caspase 8 phosphorylation essential for EMT in lung adenocarcinoma cell lines preferentially occurs in cells with the mesenchymal phenotype, resulting in chemoresistance to cisplatin plus paclitaxel in patients with resectable lung adenocarcinoma and a significantly worse 5-year PFS. Cisplatin killed lung adenocarcinoma cells regardless of caspase 8. Paclitaxel-triggered necroptosis in lung adenocarcinoma cells was dependent on the phosphorylation or deficiency of caspase 8, during which FADD interacted with RIPK1 to activate the RIPK1/RIPK3/MLKL signaling axis. Accompanied… More >

Huiling Wang^*, Xin Hu^†, Feng Yang^‡, Hui Xiao^*

Oncology Research, Vol.28, No.7-8, pp. 731-744, 2020, DOI:10.3727/096504020X16100888208039

Abstract This study was designed to investigate the precise mechanisms of miR-325-3p/S100A2 axis in breast cancer (BC). In this study, we found that the level of miR-325-3p was dramatically increased in BC tissues and cell lines, and the expression of S100A2 was significantly decreased. Also, the high level of miR-325-3p was closely associated with low expression of S100A2 in BC tissues. Moreover, introduction of miR-325-3p significantly promoted proliferation, invasion, and EMT of BC cells. Bioinformatics analysis predicted that the S100A2 was a potential target gene of miR-325-3p. Luciferase reporter assay demonstrated that miR-325-3p could directly target S100A2. In addition, miR-325-3p overexpression… More >

Kazuhiro Yamamoto^*, Takeshi Ioroi^*, Kazuaki Shinomiya^†, Ayaka Yoshida^*, Kenichi Harada^‡, Masato Fujisawa^‡, Tomohiro Omura^*, Yasuaki Ikemi^§, Shunsaku Nakagawa^§, Atsushi Yonezawa^§, Osamu Ogawa^¶, Kazuo Matsubara^§, Takuya Iwamoto^#, Kohei Nishikawa^**, Sayaka Hayashi^††, Daichi Tohara^††, Yoji Murakami^‡‡, Takanobu Motoshima^‡‡, Hirofumi Jono^††, Ikuko Yano^*§

Oncology Research, Vol.29, No.1, pp. 11-23, 2021, DOI:10.3727/096504022X16418911579334

Abstract We evaluated the association of signal transducer and activator of transcription 3 (STAT3) polymorphisms with the incidence of mammalian target of rapamycin (mTOR) inhibitor-induced interstitial lung disease (ILD) in patients with renal cell carcinoma (RCC). We also used lung-derived cell lines to investigate the mechanisms of this association. Japanese patients with metastatic RCC who were treated with mTOR inhibitors were genotyped for the STAT3 polymorphism, rs4796793 (−1697C/G). We evaluated the association of the STAT3 genotype with the incidence of ILD and therapeutic outcome. In the 57 patients included in the primary analysis, the ILD rate within 140 days was significantly… More >