Evidence map›Paper›PMID 36990974›Full record

ArticleOncogenesis2023

ACT001 inhibited CD133 transcription by targeting and inducing Olig2 ubiquitination degradation.

Huiting Deng, Hailin Liu, Guoyue Yang, Dandan Wang, Ying Luo, Chenglong Li, Zhenchang Qi, Zhili Liu, Peng Wang, Yanfang Jia and 2 more

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Effect of Transferrin-Modified FeThoracic cancer · 2025
    Article
  6. Review
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

12 authors at 2 institutions in 1 country.

Huiting DengTianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, Tianjin Third Central Hospital affiliated to Nankai University, Nankai University, 83 Jintang Road, Tianjin, 300170, People's Republic of China.
Hailin LiuDepartment of Lung Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, People's Republic of China.
Guoyue YangTianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, Tianjin Third Central Hospital affiliated to Nankai University, Nankai University, 83 Jintang Road, Tianjin, 300170, People's Republic of China.
Dandan WangTianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, Tianjin Third Central Hospital affiliated to Nankai University, Nankai University, 83 Jintang Road, Tianjin, 300170, People's Republic of China.
Ying LuoTianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, Tianjin Third Central Hospital affiliated to Nankai University, Nankai University, 83 Jintang Road, Tianjin, 300170, People's Republic of China.
Chenglong LiTianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, Tianjin Third Central Hospital affiliated to Nankai University, Nankai University, 83 Jintang Road, Tianjin, 300170, People's Republic of China.
Zhenchang QiTianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, Tianjin Third Central Hospital affiliated to Nankai University, Nankai University, 83 Jintang Road, Tianjin, 300170, People's Republic of China.
Zhili LiuTianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, Tianjin Third Central Hospital affiliated to Nankai University, Nankai University, 83 Jintang Road, Tianjin, 300170, People's Republic of China.
Peng WangTianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, Tianjin Third Central Hospital affiliated to Nankai University, Nankai University, 83 Jintang Road, Tianjin, 300170, People's Republic of China.
Yanfang JiaTianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, Tianjin Third Central Hospital affiliated to Nankai University, Nankai University, 83 Jintang Road, Tianjin, 300170, People's Republic of China.
Yingtang GaoTianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, Tianjin Third Central Hospital affiliated to Nankai University, Nankai University, 83 Jintang Road, Tianjin, 300170, People's Republic of China. gaoyt816@163.com.ORCID http://orcid.org/0000-0002-5564-1986
Yahui DingState Key Laboratory of Medicinal Chemical Biology, College of Chemistry, Nankai University, Haihe Education Park, 38 Tongyan Road, Tianjin, 300353, People's Republic of China. 017095@nankai.edu.cn.ORCID http://orcid.org/0000-0001-8588-7728
Nankai University · CNTianjin Medical University Cancer Institute and Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81903456Natural Science Foundation of Tianjin City (Natural Science Foundation of Tianjin) 20JCQNJC00960Natural Science Foundation of Tianjin City (Natural Science Foundation of Tianjin) 20JCQNJC02080
6 · The paper itself

Abstract

Lung cancer is the most lethal malignancies with high aggressive and poor prognosis. Until now, the five-year survival rate has not been improved which brings serious challenge to human health. Lung cancer stem cells (LCSCs) serve as the root of cancer occurrence, progression, recurrence, and drug resistance. Therefore, effective anti-cancer agents and molecular mechanisms which could specifically eliminate LCSCs are urgently needed for drug design. In this article, we discovered Olig2 was overexpressed in clinical lung cancer tissues and acted as a transcription factor to regulate cancer stemness by regulating CD133 gene transcription. The results suggested Olig2 could be a promising target in anti-LCSCs therapy and new drugs targeted Olig2 may exhibit excellent clinical results. Furthermore, we verified ACT001, a guaianolide sesquiterpene lactone in phase II clinical trial with excellent glioma remission, inhibited cancer stemness by directly binding to Olig2 protein, inducing Olig2 ubiquitination degradation and inhibiting CD133 gene transcription. All these results suggested that Olig2 could be an excellent druggable target in anti-LCSCs therapy and lay a foundation for the further application of ACT001 in the treatment of lung cancer in clinical.

Identifiers

PMID36990974
PMCPMC10060425
OpenAlexW4361277699

What OpenQuestion holds

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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.