Evidence map›Paper›PMID 30999914›Full record

ArticleMolecular cancer2019

Ai-lncRNA EGOT enhancing autophagy sensitizes paclitaxel cytotoxicity via upregulation of ITPR1 expression by RNA-RNA and RNA-protein interactions in human cancer.

Shouping Xu, Peiyuan Wang, Jian Zhang, Hao Wu, Shiyao Sui, Jinfeng Zhang, Qin Wang, Kun Qiao, Weiwei Yang, Hongbiao Xu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
6.3field-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

84 citing papers in PubMed, 127 citations in OpenAlex.

  1. Trial
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  3. lncRNA EGOT across cancers: TCGA analysis.Archives of medical science : AMS · 2026
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  8. lncRNABiomedicines · 2025
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  13. The Role of Long Non-Coding RNAs in Ovarian Cancer Cells.International journal of molecular sciences · 2024
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24 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

11 authors at 1 institution in 1 country.

Shouping XuDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, China.
Peiyuan WangDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, China.
Jian ZhangDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, China.
Hao WuDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, China.
Shiyao SuiDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, China.
Jinfeng ZhangDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, China.
Qin WangDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, China.
Kun QiaoDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, China.
Weiwei YangDepartment of Pathology, Harbin Medical University, Harbin, China.
Hongbiao XuDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, China.
Da PangDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, China. pangda@ems.hrbmu.edu.cn.ORCID 0000-0003-2853-4170
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe biology function of antisense intronic long noncoding RNA (Ai-lncRNA) is still unknown. Meanwhile, cancer patients with paclitaxel resistance have limited therapeutic options in the clinic. However, the potential involvement of Ai-lncRNA in paclitaxel sensitivity remains unclear in human cancer.

methodsWhole transcriptome sequencing of 33 breast specimens was performed to identify Ai-lncRNA EGOT. Next, the role of EGOT in regulation of paclitaxel sensitivity was investigated. Moreover, the mechanism of EGOT enhancing autophagy sensitizes paclitaxel cytotoxicity via upregulation of ITPR1 expression by RNA-RNA and RNA-protein interactions was investigated in detail. Furthermore, upstream transcriptional regulation of EGOT expression was also investigated by co-immunoprecipitation and chromatin immunoprecipitation. Finally, clinical breast specimens in our cohort, TCGA and ICGC were applied to validate the role of EGOT in enhancing of paclitaxel sensitivity.

resultsEGOT enhances autophagosome accumulation via the up-regulation of ITPR1 expression, thereby sensitizing cells to paclitaxel toxicity. Mechanistically, on one hand, EGOT upregulates ITPR1 levels via formation of a pre-ITPR1/EGOT dsRNA that induces pre-ITPR1 accumulation to increase ITPR1 protein expression in cis. On the other hand, EGOT recruits hnRNPH1 to enhance the alternative splicing of pre-ITPR1 in trans via two binding motifs in EGOT segment 2 (324-645 nucleotides) in exon 1. Moreover, EGOT is transcriptionally regulated by stress conditions. Finally, EGOT expression enhances paclitaxel sensitivity via assessment of cancer specimens.

conclusionsThese findings broaden comprehensive understanding of the biology function of Ai-lncRNAs. Proper regulation of EGOT may be a novel synergistic strategy for enhancing paclitaxel sensitivity in cancer therapy.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAnimalsAntineoplastic Agents, PhytogenicAutophagosomesAutophagyBreast NeoplasmsCell Line, TumorDrug Resistance, NeoplasmFemaleHeterogeneous-Nuclear Ribonucleoprotein Group F-HHumansInositol 1,4,5-Trisphosphate ReceptorsMiceMice, NudeAntineoplastic Agents, PhytogenicEGOT lncRNA, humanHeterogeneous-Nuclear Ribonucleoprotein Group F-HInositol 1,4,5-Trisphosphate ReceptorsITPR1 protein, humanPaclitaxelRNA, Double-StrandedRNA, Long NoncodingRNA, Small InterferingAi-lncRNAAutophagyCancerEGOTITPR1Paclitaxel

Identifiers

PMID30999914
PMCPMC6471868
OpenAlexW2939650949

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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.