ZiJun Liao^*†, Qi Zheng^†, Ting Wei^‡, YanBing Zhang^†, JieQun Ma^†, Zheng Zhao^§, HaiFeng Sun^§, KeJun Nan^*

Oncology Research, Vol.28, No.2, pp. 147-159, 2020, DOI:10.3727/096504019X15732109856009

Abstract MicroRNAs (miRNAs) play crucial roles in tumorigenesis and tumor progression. miR-561 has been reported to be downregulated in gastric cancer and affects cancer cell proliferation and metastasis. However, the role and underlying molecular mechanism of miR-561 in human non-small cell lung cancer (NSCLC) remain unknown and need to be further elucidated. In this study, we discovered that miR-561 expression was downregulated in human NSCLC tissues and cell lines. The overexpression of miR-561 inhibited NSCLC cell proliferation and cell cycle G1 /S transition and induced apoptosis. The inhibition of miR-561 facilitated cell proliferation and G1 /S transition and suppressed apoptosis. miR-561… More >

Yangmei Zhang^*1, Xichang Zhou^†1, Long Cheng^†, Xiang Wang^*, Qinglin Zhang^‡, Youwei Zhang^*, Sanyuan Sun^*

Oncology Research, Vol.28, No.3, pp. 213-223, 2020, DOI:10.3727/096504019X15668125347026

Abstract PRKAA1 (protein kinase AMP-activated catalytic subunit 1) is a catalytic subunit of AMP-activated protein kinase (AMPK), which plays a key role in regulating cellular energy metabolism through phosphorylation, and genetic variations in the PRKAA1 have been found to be associated with gastric cancer risk. However, the effect and underlying molecular mechanism of PRKAA1 on gastric cancer tumorigenesis, especially the proliferation and apoptosis, are not fully understood. Our data showed that PRKAA1 is highly expressed in BGC- 823 and MKN45 cells and is expressed low in SGC-7901 and MGC-803 cells in comparison with the other gastric cancer cells. PRKAA1 downregulation by… More >

Wenwei Jiang^*, Xinyu Cai^*, Tianyang Xu^*, Kaiyuan Liu^*, Dong Yang^*, Lin Fan^*, Guodong Li^*, Xiao Yu^†

Oncology Research, Vol.28, No.4, pp. 409-421, 2020, DOI:10.3727/096504020X15868639303417

Abstract Osteosarcoma (OS), the most common bone cancer, causes high morbidity in children and young adults. TRIM46 is a member of the family of tripartite motif (TRIM)-containing proteins that serve as important regulators of tumorigenesis. Here we investigate the possible role of TRIM46 in OS and the underlying molecular mechanism. We report an increase in the expression of TRIM46 in OS and its association with tumor size, Enneking’s stage, and patient prognosis. TRIM46 knockdown inhibits OS cell viability and cell cycle progression and induces apoptosis, while TRIM46 overexpression exerts inverse effects, which are inhibited by peroxisome proliferator-activated receptor alpha (PPAR )… More >

Yun Qin^*, Yu Wang^†‡§, Dongbo Liu^¶

Oncology Research, Vol.28, No.4, pp. 357-369, 2020, DOI:10.3727/096504020X15844389264424

Abstract It has been reported that kindlin-3 expression is closely associated with progression of many cancers and microRNA (miRNA) processing. However, the effects and precise mechanisms of kindlin-3 in acute myeloid leukemia (AML) have not been well clarified. Our study aimed to explore the interaction between kindlin-3 and miR-4792 in AML. In our study, we found that the expression of kindlin-3 was dramatically increased in AML samples and cell lines, and the miR-4792 level was significantly downregulated. Interestingly, the low miR-4792 level was closely associated with upregulated kindlin-3 expression in AML samples. Moreover, introduction of miR-4792 dramatically suppressed proliferation and invasion… More >

Qiuyun Luo^*†1, Wentao Pan^*†‡1, Suna Zhou^*†1, Guangfeng Wang^‡, Hanjie Yi^*§, Lin Zhang^*¶, Xianglei Yan^*†, Luping Yuan^*†, Zhenyi Liu^#, Jing Wang^**, Haibo Chen^#, MiaoZhen Qiu^*††, DaJun Yang^*†‡, Jian Sun^*‡‡

Oncology Research, Vol.28, No.4, pp. 331-344, 2020, DOI:10.3727/096504020X15825405463920

Abstract Despite therapeutic advances, the effective treatment for relapsed or refractory diffuse large B-cell lymphoma (DLBCL) remains a major clinical challenge. Evasion of apoptosis through upregulating antiapoptotic B-cell lymphoma-2 (BCL-2) family members and p53 inactivation, and abnormal activation of B-cell receptor signaling pathway are two important pathogenic factors for DLBCL. In this study, our aim is to explore a rational combination of BCL-2 inhibitor plus Bruton’s tyrosine kinase (BTK) blockade or p53 activation for treating DLBCL with the above characteristics. We demonstrated that a novel BCL-2 selective inhibitor APG-2575 effectively suppressed DLBCL with BCL-2 high expression via activating the mitochondrial apoptosis… More >

Fen Liu^*†, Shaojun Liu^*, Feiyan Ai^*†, Decai Zhang^*†, Zhiming Xiao^*, Xinmin Nie^‡, Yunfeng Fu^§

Oncology Research, Vol.28, No.5, pp. 553-557, 2020, DOI:10.3727/096504020X16032056440094

Abstract Colorectal cancer (CRC) is one of the most common malignancies in the world, with a high incidence and a high mortality. However, the pathogenesis of CRC carcinogenesis is still unexplored. In this study, we investigated the role of miR-107 in the regulation of CRC cell proliferation and apoptosis. First, the expression of miR-107 was observed to be aberrantly increased in human CRC tumor tissues and cell lines when compared to the colonic control tissues and colon epithelial cells. Further study showed that the proliferative and apoptotic capacities of human CRC SW480 and LoVo cells were aberrantly regulated by miR-107. The… More >

Leonard Lothstein^*, Judith Soberman^†, Deanna Parke^*, Jatin Gandhi^*, Trevor Sweatman^‡, Tiffany Seagroves^*

Oncology Research, Vol.28, No.5, pp. 451-465, 2020, DOI:10.3727/096504020X15898794315356

Abstract Triple-negative breast cancer (TNBC) is unresponsive to antiestrogen and anti-HER2 therapies, requiring the use of cytotoxic drug combinations of anthracyclines, taxanes, cyclophosphamide, and platinum compounds. Multidrug therapies achieve pathological cure rates of only 20–40%, a consequence of drug resistance and cumulative dose limitations necessitated by the reversible cardiotoxic effects of drug therapy. Safer and more effective treatments for TNBC are required to achieve durable therapeutic responses. This study describes the mechanistic analyses of the novel anthracycline, pivarubicin, and its in vivo efficacy against human primary TNBC. Pivarubicin directly activates PKCd, triggers rapid mitochondrial-dependent apoptosis, and circumvents resistance conferred by overexpression… More >

Lili Deng^*1, Xue Yang^†1, Jun Fan^*, Yuedi Ding^*, Ying Peng^*, Dong Xu^*, Biao Huang^*‡, Zhigang Hu^†

Oncology Research, Vol.28, No.6, pp. 579-590, 2020, DOI:10.3727/096504020X15942028641011

Abstract Colorectal cancer is an aggressive malignancy for which there are limited treatment options. Oncolytic vaccinia virus is being developed as a novel strategy for cancer therapy. Arming vaccinia virus with immunostimulatory cytokines can enhance the tumor cell-specific replication and antitumor efficacy. Interleukin-24 (IL-24) is an important immune mediator, as well as a broad-spectrum tumor suppressor. We constructed a targeted vaccinia virus of Guang9 strain harboring IL-24 (VG9-IL-24) to evaluate its antitumor effects. In vitro, VG9-IL-24 induced an increased number of apoptotic cells and blocked colorectal cancer cells in the G₂ /M phase of the cell cycle. VG9-IL-24 induced apoptosis in… More >

Tao Wang, Fan Shi, JiQuan Wang, Zi Liu, Jin Su

Oncology Research, Vol.28, No.9, pp. 969-970, 2020, DOI:10.3727/096504022X16414984936773

Abstract Kallistatin has been recognized as an endogenous angiogenesis inhibitor and exerts pleiotropic effects in inhibiting tumor growth, migration, apoptosis, and inflammation. The purpose of the present study was to investigate the potential role and mechanisms of kallistatin in cervical cancer. We demonstrated that kallistatin effectively inhibited cell proliferation and enhanced apoptosis in a dose-dependent manner. Additionally, kallistatin suppressed migration and invasion activities and markedly reduced the expression of matrix-degrading metalloproteinases, progelatinase (MMP-2), MMP-9, and urokinase-type PA (uPA). Kallistatin reversed the epithelial–mesenchymal transition (EMT) and caused the upregulation of epithelial markers such as E-cadherin and inhibited mesenchymal markers such as N-cadherin… More >

HAIYANG CHEN^1,2,#, JINGYAO SU^1,#, DANYANG CHEN^1,#, YUYE DU¹, RUILIN ZHENG¹, QINGLIN DENG², QIANQIAN DU³, BING ZHU^1,*, YINGHUA LI^1,*

BIOCELL, Vol.46, No.10, pp. 2267-2273, 2022, DOI:10.32604/biocell.2022.020218

Abstract At present, Hepatocarcinoma is one of the main causes of tumor related death all over the world. However, there are still many clinical restrictions on the treatment of liver cancer. Recently, L-Selenocystine has been shown to be a novel treatment for tumors, especially human glioma cells. But, the mechanism of L-Selenocystine against hepatocellular carcinoma remains unclear. Therefore, the main objective of this study was to investigate the effects of L-Selenocystine on HepG2 cell proliferation and activation of reactive oxygen species (ROS) mediated signaling pathway. L-Selenocystine can significantly inhibit HepG2 cell proliferation by activating caspase-3 and cleaving PARP to induce apoptosis.… More >