Evidence map›Paper›PMID 35487890›Full record

ArticleOncogenesis2022

Neuron-specific enolase promotes stem cell-like characteristics of small-cell lung cancer by downregulating NBL1 and activating the BMP2/Smad/ID1 pathway.

Lin Lu, Zhiqiang Zha, Peiling Zhang, Peipei Wang, Xia Liu, Xisheng Fang, Chengyin Weng, Baoxiu Li, Haibo Mao, Lina Wang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Neuron-Specific Enolase-What Are We Measuring?International journal of molecular sciences · 2024
    Review
  13. Article
  14. BeyondMolecular therapy oncolytics · 2023
    Review
  15. Article
  16. Article
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

15 authors at 4 institutions in 2 countries.

Lin Lu *Department of Medical Oncology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.
Zhiqiang Zha *Department of Medical Oncology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0003-3292-0947
Peiling Zhang *Department of Medical Oncology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0002-5316-6712
Peipei Wang *Department of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, 510180, Guangzhou, Guangdong, China.
Xia LiuDepartment of Medical Oncology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0002-9350-8203
Xisheng FangDepartment of Medical Oncology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0002-9507-3100
Chengyin WengDepartment of Medical Oncology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.
Baoxiu LiDepartment of Medical Oncology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.
Haibo MaoDepartment of Medical Oncology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.
Lina WangDepartment of Medical Oncology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0003-0768-0638
Mingmei GuanDepartment of Medical Oncology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0002-3294-2444
Yong WuDepartment of Medical Oncology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0002-7874-3547
Zhixiang XuDivision of Hematology and Oncology, Comprehensive Cancer Center, the University of Alabama at Birmingham, Birmingham, AL, 35233, USA. zhixiangxu@uabmc.edu.ORCID http://orcid.org/0000-0002-2385-3044
Zhongqiu LiuInternational Institute for Translational Chinese Medicine, Guangzhou University of Chinese Medicine, 510006, Guangzhou, Guangdong, China. liuzq@gzucm.edu.cn.ORCID http://orcid.org/0000-0001-6986-9677
Guolong LiuDepartment of Medical Oncology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China. eyglliu@scut.edu.cn.ORCID http://orcid.org/0000-0002-8336-1703
Guangzhou First People's Hospital · CNFirst Affiliated Hospital of Guangzhou Medical University · CNGuangzhou University of Chinese Medicine · CNUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Little is known about the biological functions of neuron-specific enolase (NSE) as a specific biomarker for small-cell lung cancer (SCLC). Herein, we elucidate the effect and mechanism of NSE on SCLC stem cell-like characteristics. Upregulated NSE expression was observed in spheroid cells. The gain-of-function and loss-of-function approaches demonstrated that modulation of NSE positively regulated cell proliferation, drug resistance, spherical clone formation, tumor growth, and stem cell-like characteristics of SCLC cells. Mechanistic studies revealed that NSE might downregulate the expression of neuroblastoma suppressor of tumorigenicity 1 (NBL1) by interacting with NBL1, thereby attenuating the competitive inhibitory effect of NBL1 on BMP2 and enhancing the interaction between BMP2 and BMPR1A; this, in turn, may activate the BMP2/Smad/ID1 pathway and promote SCLC stem cell-like characteristics. Moreover, overexpression of NBL1or knockdown of BMP2 rescued the NSE-induced stem cell-like characteristics. In clinical specimens, NSE expression was positively associated with ALDH1A1 expression and negatively correlated with NBL1 expression. High NSE and ALDH1A1 expressions and low NBL1 expression were correlated with poor prognosis in patients with SCLC. In summary, our study demonstrated that NSE promoted stem cell-like characteristics of SCLC via NBL1 and the activation of the BMP2/Smad/ID1 pathway.

Identifiers

PMID35487890
PMCPMC9054797
OpenAlexW4225159741

What Socratic 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 Socratic graph.