Evidence map›Paper›PMID 31718693›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

Long non-coding RNA RP11-468E2.5 curtails colorectal cancer cell proliferation and stimulates apoptosis via the JAK/STAT signaling pathway by targeting STAT5 and STAT6.

Li Jiang, Xu-Hai Zhao, Yin-Ling Mao, Jun-Feng Wang, Hui-Jun Zheng, Qing-Shan You

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
7.0field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

70 citing papers in PubMed, 144 citations in OpenAlex.

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  4. CDCA4 promotes bladder cancer progression by JAK/STAT signaling pathway.Journal of cancer research and clinical oncology · 2025
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10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Li JiangDepartment of Hematology and Lymphatic Diseases, Harbin Medical University Tumour Hospital, Harbin, 150081, People's Republic of China.
Xu-Hai ZhaoDepartment of Breast Surgery, Harbin Medical University Tumour Hospital, Harbin, 150081, People's Republic of China.
Yin-Ling MaoDepartment of Abdominal Radiotherapy, Harbin Medical University Tumour Hospital, No. 150, Haping Road, Nangang District, Harbin, 150081, People's Republic of China. 569655212@qq.com.
Jun-Feng WangDepartment of Thoracic Surgery, Harbin Medical University Tumour Hospital, Harbin, 150081, People's Republic of China.
Hui-Jun ZhengDepartment of General Surgery, Kangying Hospital of Mingshui County, Suihua, 151700, People's Republic of China.
Qing-Shan YouDepartment of Abdominal Radiotherapy, Harbin Medical University Tumour Hospital, No. 150, Haping Road, Nangang District, Harbin, 150081, People's Republic of China.
Harbin Medical University · CNThird Affiliated Hospital of Harbin Medical University · CN

Funding

Effects of long non-coding RNA ANRIL on proliferation, apoptosis and autophagy of diffuse large B-cell lymphoma cells via the NF-κB signaling pathway LH2019H101
6 · The paper itself

Abstract

backgroundLong non-coding RNAs (lncRNAs) are tumor-associated biological molecules and have been found to be implicated in the progression of colorectal cancer (CRC). This study aims to examine the effects of lncRNA RP11-468E2.5 and its target genes (STAT5 and STAT6) on the biological activities of CRC cells via the Janus kinase-signal transducer and activator of transcription (JAK/STAT) signaling pathway.

methodsWe initially screened the GEO database for differentially expressed lncRNAs related to CRC and then made a prediction of the implicated target genes. Then we collected CRC tissues and adjacent normal tissues from 169 CRC patients. Human CRC HCT116 and SW480 cells were treated with small interference RNA (siRNA) against RP11-468E2.5, AG490 (an inhibitor of the JAK/STAT signaling pathway), or both in combination. Next, we measured the effects of RP11-468E2.5 treatment on cellular activities such as cell viability, cycle distribution and cell apoptosis, and studied interactions among RP11-468E2.5, STAT5/STAT6, and the JAK/STAT signaling pathway. Finally, an in vivo tumor formation assay was performed to observe the effect of RP11-468E2.5 on tumor growth.

resultsThe CRC-related gene microarray data showed low expression of RP11-468E2.5 in CRC surgical specimens. However, RP11-468E2.5 was confirmed to target STAT5 and STAT6, which participate in the JAK/STAT signaling pathway. CRC tissues showed lower expression of RP11-468E2.5, higher expression of STAT5, STAT6 and of the cell cycle marker Cyclin D1 (CCND1), compared to the findings in adjacent normal tissues. The treatment of siRNA against RP11-468E2.5 increased expression of JAK2, STAT3, STAT5, STAT6, CCND1 and Bcl-2 along with the extent of STAT3, STAT5 and STAT6 phosphorylation, while lowering expression of P21 and P27. Treatment with AG490 exhibited approximately opposite effects, whereas siRNA against RP11-468E2.5 treatment stimulated CRC cell proliferation and reduced cell apoptosis, while promoting cell cycle entry; AG490 treatment reversed these results.

conclusionsAltogether, we conclude that up-regulation of RP11-468E2.5 inhibits the JAK/STAT signaling pathway by targeting STAT5 and STAT6, thereby suppressing cell proliferation and promoting cell apoptosis in CRC.

Indexed as

AdultAgedApoptosisCell ProliferationColorectal NeoplasmsHumansMiddle AgedRNA, Long NoncodingSignal TransductionSTAT5 Transcription FactorSTAT6 Transcription FactorTumor Suppressor ProteinsRNA, Long NoncodingSTAT5A protein, humanSTAT5 Transcription FactorSTAT6 protein, humanSTAT6 Transcription FactorTumor Suppressor ProteinsApoptosisColorectal cancerJanus kinase-signal transducer and activator of transcription signaling pathwayLong non-coding RNA RP11-468E2.5ProliferationSTAT5 geneSTAT6 gene

Identifiers

PMID31718693
PMCPMC6852742
OpenAlexW2985154807

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.