Evidence map›Paper›PMID 27367027›Full record

ArticleOncotarget2016

Inflammatory related gene IKKα, IKKβ, IKKγ cooperates to determine liver cancer stem cells progression by altering telomere via heterochromatin protein 1-HOTAIR axis.

Jiahui An, Mengying Wu, Xiaoru Xin, Zhuojia Lin, Xiaonan Li, Qidi Zheng, Xin Gui, Tianming Li, Hu Pu, Haiyan Li and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

11 citing papers in PubMed, 15 citations in OpenAlex.

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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.

Jiahui AnSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Mengying WuSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Xiaoru XinSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Zhuojia LinSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Xiaonan LiSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Qidi ZhengSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Xin GuiSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Tianming LiSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Hu PuSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Haiyan LiSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Dongdong LuSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Tongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem cells are associated with tumor recurrence. IKK is a protein kinase that is composed of IKKα, IKKβ, IKKγ. Herein, we demonstrate that IKKα plus IKKβ promoted and IKKγ inhibited liver cancer stem cell growth in vitro and in vivo. Mechanistically, IKKα plus IKKβ enhanced and IKKγ inhibited the interplay among HP1α, HP1β and HP1γ that competes for the interaction among HP1α, SUZ12, HEZ2. Therefore, IKKα plus IKKβ inhibited and IKKγ enhanced the activity of H3K27 methyltransferase SUZ12 and EZH2, which methylates H3K27 immediately sites on HOTAIR promoter region. Therefore, IKKα plus IKKβ increased and IKKγ decreased the HOTAIR expression. Strikingly, IKKα plus IKKβ decreases and IKKγ increases the HP1α interplays with DNA methyltransferase DNMT3b, which increases or decreases TERRA promoter DNA methylation. Thus IKKα plus IKKβ reduces and IKKγ increases to recruit TRF1 and RNA polymerase II deposition and elongation on the TERRA promoter locus, which increases or decreases TERRA expression. Furthermore, IKKα plus IKKβ decreases/increases and IKKγ increases/decreases the interplay between TERT and TRRRA/between TERT and TREC. Ultimately, IKKα plus IKKβ increases and IKKγ decreases the telomerase activity. On the other hand, at the telomere locus, IKKα plus IKKβ increases/drcreases and IKKγ decreases/increases TRF2, POT1, pPOT1, Exo1, pExo1, SNM1B, pSNM1B/CST-AAF binding, which keep active telomere regulatory genes and poised for telomere length. Strikingly, HOTAIR is required for IKKα plus IKKβ and IKKγ to control telomerase activity and telomere length. These observations suggest that HOTAIR operates the action of IKKα, IKKβ, IKKγ in liver cancer stem cells. This study provides a novel basis to elucidate the oncogenic action of IKKα, IKKβ, IKKγ and prompts that IKKα, IKKβ, IKKγ cooperate to HOTAR to be used as a novel therapeutic targets for liver cancer.

Indexed as

AnimalsCell MovementChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDisease ProgressionDNA MethylationGene Expression Regulation, NeoplasticHistonesHumansI-kappa B KinaseInflammationLiver NeoplasmsMiceMice, Inbred BALB CNeoplasm Recurrence, LocalNeoplasm TransplantationCBX1 protein, humanCBX5 protein, humanChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneCHUK protein, humanHistonesHOTAIR long untranslated RNA, humanI-kappa B KinaseIKBKB protein, humanIKBKG protein, humanRNA, Long NoncodingHOTAIRIKKαIKKβIKKγtelomere

Identifiers

PMID27367027
PMCPMC5226573
OpenAlexW2462258096

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.