Evidence mapPaperPMID 36823149Full record

ArticleCell death & disease2023

HOXC11 drives lung adenocarcinoma progression through transcriptional regulation of SPHK1.

Xin Peng, Xiaoli Liu, Wanshan Hu, Yanling Zhou, Lianlian Ouyang, Xintong Peng, Yao Long, Jingyue Sun, Tania Tao, Ling Chen and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 9 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

14 authors at 1 institution in 3 countries.

Xin PengDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.ORCID 0000-0003-0601-4991
Xiaoli LiuNHC Key Laboratory of Carcinogenesis of Ministry of Health (Central South University), Cancer Research Institute; School of Basic Medicine, Central South University, Changsha, Hunan, 410008, China.
Wanshan HuDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Yanling ZhouDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Lianlian OuyangNHC Key Laboratory of Carcinogenesis of Ministry of Health (Central South University), Cancer Research Institute; School of Basic Medicine, Central South University, Changsha, Hunan, 410008, China.
Xintong PengDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Yao LongDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Jingyue SunDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Tania TaoDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Ling ChenNHC Key Laboratory of Carcinogenesis of Ministry of Health (Central South University), Cancer Research Institute; School of Basic Medicine, Central South University, Changsha, Hunan, 410008, China.
Ying ShiNHC Key Laboratory of Carcinogenesis of Ministry of Health (Central South University), Cancer Research Institute; School of Basic Medicine, Central South University, Changsha, Hunan, 410008, China.ORCID 0000-0003-4671-4896
Yongguang TaoDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.ORCID 0000-0003-2354-5321
Desheng XiaoDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China. xdsh96@csu.edu.cn.ORCID 0000-0003-2204-5042
Shuang LiuDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China. shuangliu2016@csu.edu.cn.ORCID 0000-0002-7206-7277
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung adenocarcinoma (LUAD) is a fatal threat to human health, while the mechanism remains unclear, and the therapy brings limited therapeutic effects. Transcription factor Homeobox C11 (HOXC11) was previously proved to be related to hind limbs and metanephric development during the embryonic phase, and its role in tumors has been gradually recognized. Our study found that HOXC11 overexpressed in LUAD and was associated with worse overall survival. Moreover, its expression in lung cancer was regulated by IκB kinase α (IKKα), a pivotal kinase in NF-κB signaling, which was related to the ubiquitination of HOXC11. We further proved that HOXC11 could enhance the ability of proliferation, migration, invasion, colony formation, and the progression of the cell cycle in LUAD cells. Meanwhile, it also accelerated the formation of subcutaneous and lung metastases tumors. In contrast, loss of HOXC11 in LUAD cells significantly inhibited these malignant phenotypes. At the same time, HOXC11 regulated the expression of sphingosine kinase 1 (SPHK1) by directly binding to its promoter region. Therefore, we conclude that HOXC11 impacts the development of LUAD and facilitates lung cancer progression by promoting the expression of SPHK1.

Indexed as

Adenocarcinoma of LungHomeodomain ProteinsLung NeoplasmsPhosphotransferases (Alcohol Group Acceptor)Cell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansSphingosine KinaseHomeodomain ProteinsHOXC11 protein, humanPhosphotransferases (Alcohol Group Acceptor)Sphingosine Kinase

Identifiers

PMID36823149
PMCPMC9950477
OpenAlexW4321607496

What Socratic 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 Socratic graph.