Evidence map›Paper›PMID 39732937›Full record

ArticleScientific reports2024

CHD1L accelated the progression of cutaneous squamous cell carcinoma via promoting PI3K/PD-L1 signaling pathway induced M2 polarization of TAMs.

Mei Liu, Chao Lv, Haiping Dong, Meng Zhou, Yao Yao, Huanrong Hu, Na Shen, Baoguo Liu, Guoying Miao, Yaling Liu

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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

10 authors.

Mei LiuDepartment of Dermatology, Hebei Medical University Third Hospital, 139 Ziqiang Road, Shijiazhuang, 050000, Hebei, China.
Chao LvDepartment of Dermatology, Affiliated Hospital of Hebei University of Engineering, No. 81 Congtai Road, Handan, 056000, Hebei, China.
Haiping DongDepartment of Oncology, Handan First Hospital, No. 25 Congtai Road, Handan, 056000, Hebei, China.
Meng ZhouDepartment of Dermatology, Affiliated Hospital of Hebei University of Engineering, No. 81 Congtai Road, Handan, 056000, Hebei, China.
Yao YaoDepartment of Science and Education, Affiliated Hospital of Hebei University of Engineering, No. 81 Congtai Road, Handan, 056000, Hebei, China.
Huanrong HuDepartment of Dermatology, Hebei Medical University Third Hospital, 139 Ziqiang Road, Shijiazhuang, 050000, Hebei, China.
Na ShenDepartment of Science and Education, Affiliated Hospital of Hebei University of Engineering, No. 81 Congtai Road, Handan, 056000, Hebei, China.
Baoguo LiuDepartment of Dermatology, Affiliated Hospital of Hebei University of Engineering, No. 81 Congtai Road, Handan, 056000, Hebei, China.
Guoying MiaoDepartment of Dermatology, Affiliated Hospital of Hebei University of Engineering, No. 81 Congtai Road, Handan, 056000, Hebei, China.
Yaling LiuDepartment of Dermatology, Hebei Medical University Third Hospital, 139 Ziqiang Road, Shijiazhuang, 050000, Hebei, China. 18230202166@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate CHD1L's impacts and molecular processes in hypoxic cutaneous squamous cell carcinoma. Monoclonal proliferation assays and CCK-8 were used to detect the proliferation capacity of A431 cells and Colon16 cells; wound healing experiments and Transwell assays were used to examine the migration and invasion capacity of A431 cells and Colon16 cells; angiogenesis experiments were conducted to assess the influence of A431 cells on angiogenesis; a nude mouse tumor xenograft experiment and HE staining were utilized to evaluate the impact of CHD1L on the progression of cutaneous squamous cell carcinoma; western blot analysis was performed to detect the expression of p-PI3K, p-AKT, and PD-L1 in A431 cells, as well as CD9, TSG101, PD-L1 in exosomes, and CD206, Arginase-1, iNOS, IL-1β, p-AKT, p-mTOR, VEGF, COX-2, MMP2, MMP9, p-ERK1/2 in tumor-associated macrophages. Under hypoxic conditions, CHD1L promoted the proliferation, migration, invasion, and angiogenesis of cutaneous squamous cell carcinoma. Furthermore, CHD1L facilitated the progression of cutaneous squamous cell carcinoma. CHD1L also increased the relative protein expression of p-PI3K, p-AKT, and PD-L1 in A431 cells, as well as CD9, TSG101, PD-L1 in exosomes, CD206, Arginase-1, p-AKT, p-mTOR, VEGF, COX-2, MMP2, MMP9, and p-ERK1/2 in tumor-associated macrophages, while inhibiting the relative protein expression of iNOS and IL-1β. Under hypoxic conditions, CHD1L can promote the proliferation and migration of cutaneous squamous cell carcinoma.

Indexed as

B7-H1 AntigenCarcinoma, Squamous CellCell MovementCell ProliferationDNA HelicasesPhosphatidylinositol 3-KinasesSignal TransductionSkin NeoplasmsAnimalsCell Line, TumorDisease ProgressionDNA-Binding ProteinsHumansMiceMice, NudeNeovascularization, PathologicB7-H1 AntigenCD274 protein, humanDNA-Binding ProteinsDNA HelicasesPhosphatidylinositol 3-KinasesCHD1LCutaneous squamous cell carcinomaHypoxiaTumor-associated macrophages

Identifiers

PMID39732937
PMCPMC11682224

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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.