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  • Open Access

    ARTICLE

    MicroRNA-92a Promotes Cell Proliferation in Cervical Cancer via Inhibiting p21 Expression and Promoting Cell Cycle Progression

    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 >

  • Open Access

    ARTICLE

    Long Noncoding RNA CRNDE/PRC2 Participated in the Radiotherapy Resistance of Human Lung Adenocarcinoma Through Targeting p21 Expression

    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 >

  • Open Access

    ARTICLE

    Knockdown of IARS2 Inhibited Proliferation of Acute Myeloid Leukemia Cells by Regulating p53/p21/PCNA/eIF4E Pathway

    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 >

  • Open Access

    ARTICLE

    RPSAP52 lncRNA Inhibits p21Waf1/CIP Expression by Interacting With the RNA Binding Protein HuR

    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 >

  • Open Access

    ARTICLE

    On p21 Tracking Property in Cancer Cell Unravelled Bio-Digitally in silico. Are Apoptosis Principles Universal?

    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 >

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