Evidence map›Paper›PMID 33854635›Full record

ArticleJournal of Cancer2021

SAA1 knockdown promotes the apoptosis of glioblastoma cells via downregulation of AKT signaling.

Huikai Zhang, Yang Xu, Gang Deng, Fanen Yuan, Yinqiu Tan, Lun Gao, Qian Sun, Yangzhi Qi, Kun Yang, Rongxin Geng and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. 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

13 authors at 2 institutions in 1 country.

Huikai ZhangDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Yang XuDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Gang DengDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Fanen YuanDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Yinqiu TanDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Lun GaoDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Qian SunDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Yangzhi QiDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Kun YangDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Rongxin GengDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Hongxiang JiangDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Baohui LiuDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Qianxue ChenDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Wuhan University · CNRenmin Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serum amyloid A1 (SAA1) is an inflammatory associated high-density lipoprotein. And It is also considered as a predictor and prognostic marker of cancer risk. However, its role and mechanisms in glioblastoma (GBM) still unclear. In this study, we validate that SAA1 is up-regulated in GBM, and its high expression predicts poor prognosis. SAA1 knockdown promotes the apoptosis of GBM cell. Mechanistically, SAA1 knockdown can inhibit serine/threonine protein kinase B (AKT) phosphorylation, thereby regulating the expression of apoptosis-related proteins such as Bcl2 and Bax, leading to GBM cell death. Moreover, Gliomas with low SAA1 expression have increased sensitivity to Temozolomide (TMZ). Low SAA1 expression segregated glioma patients who were treated with Temozolomide (TMZ) or with high MGMT promoter methylation into survival groups in TCGA and CGGA dataset. Our study strongly suggested that SAA1 was a regulator of cells apoptosis and acted not only as a prognostic marker but also a novel biomarker of sensitivity of glioma to TMZ.

Indexed as

AKTApoptosisGlioblastomaSerum amyloid A1Temozolomide.

Identifiers

PMID33854635
PMCPMC8040715
OpenAlexW3138539981

What OpenQuestion 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 OpenQuestion graph.