Evidence map›Paper›PMID 31274247›Full record

ArticleCancer medicine2019

Selenoprotein M stimulates the proliferative and metastatic capacities of renal cell carcinoma through activating the PI3K/AKT/mTOR pathway.

Hao Jiang, Qian-Qian Shi, Li-Yuan Ge, Qian-Feng Zhuang, Dong Xue, Hai-Yan Xu, Xiao-Zhou He

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. "Alphabet" Selenoproteins: Their Characteristics and Physiological Roles.International journal of molecular sciences · 2023
    Review
  5. Deciphering the Role of Selenoprotein M.Antioxidants (Basel, Switzerland) · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
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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

7 authors at 2 institutions in 1 country.

Hao JiangDepartment of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, People's Republic of China.ORCID 0000-0002-0660-9787
Qian-Qian ShiDepartment of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, People's Republic of China.
Li-Yuan GeDepartment of Urology, Peking University Third Hospital, Beijing, People's Republic of China.
Qian-Feng ZhuangDepartment of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, People's Republic of China.
Dong XueDepartment of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, People's Republic of China.
Hai-Yan XuDepartment of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, People's Republic of China.
Xiao-Zhou HeDepartment of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, People's Republic of China.
Soochow University · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-throughput sequencing methods have facilitated the identification of novel selenoproteins, which exert a vital role in the development and progression of tumor diseases. Recently, Selenoprotein M (SELM) is upregulated in several types of cancer. However, the biological roles of SELM in renal cell carcinoma (RCC) remain unclear. In this paper, quantitative reverse transcription PCR (qRT-PCR) and Western blot were used to measure relative levels of SELM in a cohort of RCC tissues with matched normal tissues as well as human RCC cell lines. SELM expression was found to be upregulated in RCC. High level of SELM was related to poor prognosis of RCC. Furthermore, silence of SELM could inhibit the in vitro proliferative, migratory, and invasive capacities of RCC. In addition, downregulated SELM could impede in vivo tumorigenesis of RCC. SELM could activate the PI3K/Akt/mTOR pathway and mediate expressions of matrix metallopeptidase 2 and 9 (MMP2, MMP9). In conclusion, our study reveals the oncogenic function of SELM in RCC, and SELM may be a therapeutic and prognostic target for RCC.

Indexed as

Signal TransductionAnimalsCarcinoma, Renal CellCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansKidney NeoplasmsMaleMiceNeoplasm MetastasisNeoplasm TransplantationPhosphatidylinositol 3-KinasesPrognosisMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSelenoproteinsSELM protein, humanTOR Serine-Threonine Kinasesmigration and invasionPI3K/Akt/mTORproliferationrenal cell carcinomaSelenoprotein M

Identifiers

PMID31274247
PMCPMC6712446
OpenAlexW2954027569

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.