Evidence map›Paper›PMID 31312359›Full record

ArticleAmerican journal of translational research2019

Evaluation of calcium-binding protein A11 promotes the carcinogenesis of hypopharygeal squamous cell carcinoma via the PI3K/AKT signaling pathway.

Chengyu Wang, Chen Lin, Qilei Tao, Shuwei Zhao, Huanhai Liu, Li Li

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. New Insights into the Regulation of mTOR Signaling via CaInternational journal of molecular sciences · 2023
    Review
  4. Article
  5. Review
  6. Article
  7. The Calcium Binding Protein S100A11 and Its Roles in Diseases.Frontiers in cell and developmental biology · 2021
    Review
  8. Article
  9. 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

6 authors at 1 institution in 1 country.

Chengyu WangDepartment of Otolaryngology-Head and Neck Surgery, Changzheng Hospital, Second Military Medical University Shanghai 200003, China.
Chen LinDepartment of Otolaryngology-Head and Neck Surgery, Changzheng Hospital, Second Military Medical University Shanghai 200003, China.
Qilei TaoDepartment of Otolaryngology-Head and Neck Surgery, Changzheng Hospital, Second Military Medical University Shanghai 200003, China.
Shuwei ZhaoDepartment of Otolaryngology-Head and Neck Surgery, Changzheng Hospital, Second Military Medical University Shanghai 200003, China.
Huanhai LiuDepartment of Otolaryngology-Head and Neck Surgery, Changzheng Hospital, Second Military Medical University Shanghai 200003, China.
Li LiDepartment of Otolaryngology-Head and Neck Surgery, Changzheng Hospital, Second Military Medical University Shanghai 200003, China.
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe S100 gene family encodes low molecular weight proteins implicated in cancer progression. In the present study, we explored the effects and underlying mechanisms of calcium-binding protein A11 (S100A11 protein) in hypopharyngeal squamous cell carcinoma (HSCC).

methodsRT-qPCR and western blot analysis were used to detect the mRNA and protein expression of S100A11, EGFR, MMP2, CD44, and MMP9. CCK-8, colony formation, wound healing and transwell invasion assays were performed to evaluate the effects of S100A11 on HSCC cells.

resultsIn our study, we observed that the level of S100A11 expression was significantly upregulated in HSCC tissues and cell lines. S100A11 inhibition increased the effects of 5-Fu on FaDu cells proliferation in vitro. In addition, S100A11 inhibition decreased the migration ability of FaDu cells. Additionally, the expression of migration-related proteins including EGFR, MMP2, CD44, and MMP9 were down-regulated when S100A11 was knocked down. Moreover, the expression of phosphorylated-PI3K (p-PI3K), phosphorylated-Akt (p-Akt), phosphorylated-mTOR (p-mTOR) and BCL-2 in FaDu cells were dramatically decreased.

conclusionsOur results suggested that S100A11 could activate the PI3K/Akt/mTOR signaling pathway in HSCC tumorigenesis.

Indexed as

hypopharyngeal squamous cell carcinomamigrationPI3K/Akt/mTORS100A11

Identifiers

PMID31312359
PMCPMC6614622
OpenAlexW2991522911

What OpenQuestion holds

Textmetadata
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.