Daniela D’Angelo^*, Claudio Arra^†, Alfredo Fusco^*

Oncology Research, Vol.28, No.2, pp. 191-201, 2020, DOI:10.3727/096504019X15761465603129

Abstract Long noncoding RNAs have been recently demonstrated to have an important role in fundamental biological processes, and their deregulated expression has been found in several human neoplasias. Our group has recently reported a drastic overexpression of the long noncoding RNA (lncRNA) RPSAP52 (ribosomal protein SA pseudogene 52) in pituitary adenomas. We have shown that this lncRNA increased cell proliferation by upregulating the expression of the chromatinic proteins HMGA1 and HMGA2, functioning as a competing endogenous RNA (ceRNA) through competitively binding to microRNA-15a (miR-15a), miR-15b, and miR-16. The aim of this work was to identify further… More >

Hong Li^*1, Yaning Tian^*1, Xiang Li^*, Bin Wang^†, Dongzhi Zhai^*, Yingying Bai^*, Changhu Dong^*, Xu Chao^*‡

Oncology Research, Vol.27, No.6, pp. 673-680, 2019, DOI:10.3727/096504018X15426261956343

Abstract IARS2 encodes mitochondrial isoleucine-tRNA synthetase, which mutation may cause multiple diseases. However, the biological function of IARS2 on acute myeloid leukemia (AML) has not yet been identified. In the present study, qRT-PCR was used to determine the expression of IARS2 in K562, THP1, and HL-60 leukemia cells. Additionally the mRNA levels of IARS2 in CD34 cells and AML cells obtained from patients were detected by qRT-PCR. IARS2-shRNA lentiviral vector was established and used to infect acute myeloid leukemia HL-60 cells. qRT-PCR and Western blot analysis were employed to assess the knockdown effect of IARS2. The… More >

Ming Zhang^*, Change Gao^†, Yi Yang^*, Gaofeng Li^‡, Jian Dong^§, Yiqin Ai^*, Nan Chen^‡, Wenhui Li^*

Oncology Research, Vol.26, No.8, pp. 1245-1255, 2018, DOI:10.3727/096504017X14944585873668

Abstract Long noncoding RNAs (lncRNAs), a new class of functional regulators involved in human tumorigenesis, have been attracting the increasing attention of researchers. The lncRNA colorectal neoplasia differentially expressed (CRNDE) gene, transcribed from chromosome 16 on the strand opposite the adjacent IRX5 gene, was originally found to be increased in CRC and was reported to be abnormally expressed in many cancers. However, its potential role and the molecular mechanism underlying the radioresistant phenotype formation of lung adenocarcinoma (LAD) remain unclear. In our present study, we identified that CRNDE was significantly upregulated in LAD tissue and radioresistant… More >

Zhiying Su^*1, Hua Yang^†1, Min Zhao^*,‡ Yanlong Wang^*, Guoyi Deng^*, Ruixin Chen^*

Oncology Research, Vol.25, No.1, pp. 137-145, 2017, DOI:10.3727/096504016X14732772150262

Abstract MicroRNA-92a (miR-92a) generally plays a promoting role in human cancers, but the underlying mechanism in cervical cancer remains unclear. Here we studied the expression and clinical significance of miR-92a in cervical cancer, as well as the regulatory mechanism in the proliferation of cervical cancer cells. Our data indicated that miR-92a was significantly upregulated in cervical cancer tissues compared to their matched adjacent nontumor tissues (ANTs), and the increased miR-92a levels were significantly associated with a higher grade, lymph node metastasis, and advanced clinical stage in cervical cancer. In vitro study revealed that inhibition of miR-92a… More >

Hao Lu¹, Chaoyang Sun¹, Ting Zhou, Bo Zhou, Ensong Guo, Wanying Shan, Meng Xia, Kezhen Li, Danhui Weng, Li Meng, Xiaoyan Xu, Junbo Hu, Ding Ma, Gang Chen

Oncology Research, Vol.23, No.3, pp. 119-128, 2015, DOI:10.3727/096504015X14496932933656

Abstract Drug resistance is the leading cause of chemotherapy failure in the treatment of ovarian cancer. So far, little is known about the mechanism of chemoresistance in ovarian cancer. In this study, we explored the mechanism that HSP27 was involved in cisplatin resistance of ovarian cancer both in vitro and clinically. HSP27 protein was found to be upregulated and expressed in cisplatin-resistant ovarian cancer cell line C13*, and HSP27 siRNA transfection reversed the chemoresistance of C13*. We found that HSP27 exerted its chemoresistant role by inhibiting p21 transferring from the nucleus to the plasma through the More >

Yandong Lu^*1, Fangguo Li^*1, Tao Xu^†, Jie Sun^*1

Oncology Research, Vol.23, No.4, pp. 155-163, 2015, DOI:10.3727/096504016X14519157902681

Abstract Chondrosarcoma (CHS) is the second most common malignant bone sarcoma with increased risk of invasion and metastasis. However, the regulatory mechanisms of CHS tumorigenesis remain unknown. Here we investigated the novel role of miR-497 in regulating chondrosarcoma cell growth and cell cycle arrest. RT-PCR analysis showed that the expression of miR-497 is aberrantly downregulated in human chondrosarcoma samples and cells. After transfection with miR-497 mimic or antagomir, the proliferation and apoptosis of JJ012 and OUMS-27 chondrosarcoma cells were determined by CCK-8 assay and flow cytometric analysis, respectively. Results showed that the proliferation capacity of JJ012… More >

Huiqing Lv^*, Zhongmin Zhang^†, Yaoxia Wang^†, Chenglin Li^†, Weihong Gong^†, Xin Wang^†

Oncology Research, Vol.23, No.6, pp. 283-290, 2015, DOI:10.3727/096504016X14562725373833

Abstract Colorectal cancer (CRC) is the third most common malignancy with high mortality around the world. However, the biological mechanism of CRC carcinogenesis is not completely known. In the present study, we determined the role of miR-92a in the regulation of CRC cell motility. Expression of miR-92a is aberrantly upregulated in human CRC tissues and cultured cells, as shown by RT-PCR analysis. The effects of miR-92a on the proliferation and migration of human CRC SW620 and LoVo cells were measured by CCK-8 and Transwell assay, respectively. Results showed that the proliferation and migration capacity of both… More >

R. M. Ardito Marretta^∗,†, G. Barbaraci^‡

Molecular & Cellular Biomechanics, Vol.7, No.3, pp. 135-164, 2010, DOI:10.3970/mcb.2010.007.135

Abstract Upon severe DNA damage, p21 acts in a dual mode; on the one hand, it inhibits the cyclin-CDK complex for arresting the G2/M transition and on the other hand, it indirectly becomes an apoptotic factor by activating - in sequence - the retinoblastoma protein, E2F1 and APAF1 expressions. But, in a cancer cells proliferation, the mechanisms of, and participants in, the apoptosis failure remain unclear. Since the p21/p53/Mdm2 proteins network normally involves a digital response in a cancer cell, through an original design of a cell signalling-protein simulator, we demonstrate,in silico, that apoptosis phase instability More >