Upregulated expression of ILF2 in non-small cell lung cancer is associated with tumor cell proliferation and poor prognosis

Ni, Tianming; Mao, Guoxin; Xue, Qun; Liu, Yifei; Chen, Buyou; Cui, Xuefan; Lv, Liting; Liu, Jia; Wang, Yuchan; Ji, Lili

doi:10.1007/s10735-015-9624-5

Cited by 36 publications

(29 citation statements)

References 37 publications

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“…Previous studies have demonstrated that environmental deterioration, tobacco use, radon exposure and occupational carcinogens are risk factors for lung cancer (4)(5)(6)(7). Lung cancer is divided into two major clinically relevant groups, small cell lung cancer and non-small cell lung cancer (NSCLC), according to histological analysis (8). NSCLC is the predominant type of lung cancer and accounts for ~83% of all cases (9).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-29a functions as a potential tumor suppressor through directly targeting CDC42 in non-small cell lung cancer

Wang

et al. 2017

Oncology Letters

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Abstract. The expression and function of microRNA-29a (miR-29a) have been investigated in various types of cancer. In the present study, the expression, function and underlying molecular mechanism of miR-29a were investigated in non-small cell lung cancer (NSCLC). The expression level of miR-29a in NSCLC was determined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, migration and invasion ability were determined using Cell Counting Kit-8, cell migration and invasion assays, respectively. Bioinformatics analysis and dual-luciferase reporter assays were performed to determine whether cell division cycle 42 (CDC42) is a direct target gene of miR-29a. To assess CDC42 mRNA and protein expression following transfection with miR-29a, RT-qPCR and western blotting were performed. Following knockdown of CDC42, functional assays were performed to investigate the roles of CDC42 in NSCLC. The results demonstrated that miR-29a was downregulated in NSCLC and the decreased expression level of miR-29a was significantly associated with advanced tumor-node-metastasis classification and metastasis. In addition, upregulation of miR-29a inhibited cell proliferation, migration and invasion in NSCLC, whereas downregulation of miR-29a had the opposite effects. Furthermore, CDC42 was identified as a direct target gene of miR-29a in vitro. miR-29a was demonstrated to function as a tumor suppressor in NSCLC by directly targeting CDC42 and may be investigated further as a target therapy for NSCLC.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-29a functions as a potential tumor suppressor through directly targeting CDC42 in non-small cell lung cancer

Wang

et al. 2017

Oncology Letters

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“…In this gene set, upregulation of 27 genes was associated with poor PFS. These genes include genes that have known functions in the regulation of the ER transcriptional network (TFAP2C 18, 19 and SP1 20, 21 ), genes that have been shown to be related to breast cancer biology and clinical outcomes (TFAP2C, BMPR1A 22 , ARRDC3 23 , PPP2R3A 24 ) and genes not yet reported to be related to breast cancer but with functional roles in tumorigenesis, metastases and response to treatment in other cancer types and may also have molecular functions in breast cancer (ILF2 25 , ATP11B 26 , CSDA 27 , USP5 28 ,TANC1 29 , NOTCH2 30 , ADD3 31 and SEC23A 32 ). In addition, there are a number of genes in the gene set that do not have known roles in cancer biology (CCDC93, CPNE1, GLTP and TCEB3).…”

Section: Resultsmentioning

confidence: 99%

TransCONFIRM: Identification of a Genetic Signature of Response to Fulvestrant in Advanced Hormone Receptor–Positive Breast Cancer

Jeselsohn

Barry

Migliaccio

et al. 2016

Clinical Cancer Research

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Purpose Fulvestrant is an estrogen receptor (ER) antagonist and an approved treatment for metastatic estrogen receptor positive (ER+) breast cancer. With the exception of ER levels, there are no established predictive biomarkers of response to single agent fulvestrant. We attempted to identify a gene signature of response to fulvestrant in advanced breast cancer. Experimental Design Primary tumor samples from 134 patients enrolled in the phase III CONFIRM study of patients with metastatic ER+ breast cancer comparing treatment with either 250mg or 500mg fulvestrant were collected for genome-wide transcriptomic analysis. Gene expression profiling was performed using Affymetrix microarrays. An exploratory analysis was performed to identify biological pathways and new signatures associated with response to fulvestrant. Results Pathway analysis demonstrated that increased EGF pathway and FOXA1 transcriptional signaling is associated with decreased response to fulvestrant. Using a multivariate Cox model we identified a novel set of 37 genes whose expression is independently associated with progression free survival (PFS). TFAP2C, a known regulator of ER activity was ranked second in this gene set and high expression was associated with a decreased response to fulvestrant. The negative predictive value of TFAP2C expression at the protein level was confirmed by immunohistochemistry. Conclusions We identified biological pathways and a novel gene signature in primary ER+ breast cancers that predicts for response to treatment in the CONFIRM study. These results suggest potential new therapeutic targets and warrant further validation as predictive biomarkers of fulvestrant treatment in metastatic breast cancer.

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“…The kinetics of NF90 and NF45 chromatin association at these proximal promoters is consistent with NF90 and NF45 serving essential roles in regulating the rapid induction of IEGs that occurs on the timescale of 30 minutes to 2 hours. (26,27) and diverse cancers (28)(29)(30)(31)(32)(33).…”

Section: Discussionmentioning

confidence: 99%

“…disruption of NF90 and NF45 impaired ESC proliferation and promoted differentiation to an epiblast-like state (27). NF90 and NF45 regulate cell cycle progression (18,19,28), cell growth and proliferation (28)(29)(30)(31)(32)(33), and are amplified, overexpressed and mutated in diverse cancers (34,35).…”

Section: Introductionmentioning

confidence: 99%

Inducible expression of immediate early genes is regulated through dynamic chromatin association by NF45/ILF2and NF90/ILF3

Shi

Lowe

et al. 2018

Preprint

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Immediate early gene (IEG) transcription is rapidly activated by diverse stimuli without requiring new protein synthesis. This transcriptional regulation is assumed to involve constitutively expressed nuclear factors that are targets of signaling cascades initiated at the cell membrane. NF45 and its heterodimeric partner NF90 are chromatin-interacting proteins that are constitutively expressed and localized predominantly in the nucleus. Previously, NF90 chromatin immunoprecipitation followed by deep sequencing (ChIP-seq)

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Upregulated expression of ILF2 in non-small cell lung cancer is associated with tumor cell proliferation and poor prognosis

Cited by 36 publications

References 37 publications

MicroRNA-29a functions as a potential tumor suppressor through directly targeting CDC42 in non-small cell lung cancer

MicroRNA-29a functions as a potential tumor suppressor through directly targeting CDC42 in non-small cell lung cancer

TransCONFIRM: Identification of a Genetic Signature of Response to Fulvestrant in Advanced Hormone Receptor–Positive Breast Cancer

Inducible expression of immediate early genes is regulated through dynamic chromatin association by NF45/ILF2and NF90/ILF3

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