Evidence map›Paper›PMID 34219323›Full record

ArticleCancer science2021

RNA-binding protein SAMD4A inhibits breast tumor angiogenesis by modulating the balance of angiogenesis program.

Meicen Zhou, Bing Wang, Hongwei Li, Jianqun Han, Ailing Li, Wenbao Lu

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

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  11. Curcumin inhibits the proliferation and migration of osteosarcoma by regulating the expression of superZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
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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 2 institutions in 1 country.

Meicen Zhou *Department of Endocrinology, Beijing Jishuitan Hospital, The 4th Clinical Medical College of Peking University, Beijing, China.
Bing Wang *Institute of Microcirculation, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Hongwei LiInstitute of Microcirculation, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Jianqun HanInstitute of Microcirculation, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Ailing LiInstitute of Microcirculation, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Wenbao LuInstitute of Microcirculation, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.ORCID https://orcid.org/0000-0001-6577-3379
Chinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University · CN

Funding

CAMS Innovation Fund for Medical Science 2017-I2M-1-016National Natural Science Foundation of China 81702769Peking Union Medical College 3332017105
6 · The paper itself

Abstract

Tumor-induced angiogenesis is important for further progression of solid tumors. The initiation of tumor angiogenesis is dictated by a shift in the balance between proangiogenic and antiangiogenic gene expression programs. However, the potential mechanism controlling the expression of angiogenesis-related genes in the tumor cells, especially the process mediated by RNA-binding protein (RBP) remains unclear. SAMD4A is a conserved RBP across fly to mammals, and is believed to play an important role in controlling gene translation and stability. In this study, we identified the potential role of SAMD4A in modulating angiogenesis-related gene expression and tumor progression in breast cancer. SAMD4A expression was repressed in breast cancer tissues and cells and low SAMD4A expression in human breast tumor samples was strongly associated with poor survival of patients. Overexpression of SAMD4A inhibited breast tumor angiogenesis and caner progression, whereas knockdown of SAMD4A demonstrated a reversed effect. Mechanistically, SAMD4A was found to specifically destabilize the proangiogenic gene transcripts, including C-X-C motif chemokine ligand 5 (CXCL5), endoglin (ENG), interleukin 1β (IL1β), and angiopoietin 1 (ANGPT1), by directly interacting with the stem-loop structure in the 3' untranslated region (3'UTR) of these mRNAs through its sterile alpha motif (SAM) domain, resulting in the imbalance of angiogenic genes expression. Collectively, our results suggest that SAMD4A is a novel breast tumor suppressor that inhibits tumor angiogenesis by specifically downregulating the expression of proangiogenic genes, which might be a potential antiangiogenic target for breast cancer therapy.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBreast NeoplasmsDisease ProgressionFemaleHEK293 CellsHumansMammary Glands, HumanMCF-7 CellsMiceMice, Inbred BALB CMice, NudeNeovascularization, PathologicRepressor ProteinsRNA-Binding ProteinsTransfectionRepressor ProteinsRNA-Binding ProteinsSAMD4A protein, humanTumor Suppressor ProteinsmetastasismRNA stabilityRNA-binding proteinSAMD4Atumor angiogenesis

Identifiers

PMID34219323
PMCPMC8409301
OpenAlexW3180028523

What OpenQuestion holds

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LicenceCC BY-NC
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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.