Evidence map›Paper›PMID 32627037›Full record

ArticleOncology reports2020

Knockdown of KRT17 decreases osteosarcoma cell proliferation and the Warburg effect via the AKT/mTOR/HIF1α pathway.

Xianke Yan, Chao Yang, Wei Hu, Tao Chen, Qi Wang, Feng Pan, Bing Qiu, Bensen Tang

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

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  16. Metabolic reprogramming in osteosarcoma.Pediatric discovery · 2023
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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

8 authors at 1 institution in 1 country.

Xianke Yan *Department of Orthopedics, Guizhou Provincial Orthopedics Hospital, Guiyang, Guizhou 550000, P.R. China.
Chao Yang *Department of Orthopedics, Guizhou Provincial Orthopedics Hospital, Guiyang, Guizhou 550000, P.R. China.
Wei HuDepartment of Orthopedics, Guizhou Provincial Orthopedics Hospital, Guiyang, Guizhou 550000, P.R. China.
Tao ChenDepartment of Orthopedics, Guizhou Provincial Orthopedics Hospital, Guiyang, Guizhou 550000, P.R. China.
Qi WangDepartment of Orthopedics, Guizhou Provincial Orthopedics Hospital, Guiyang, Guizhou 550000, P.R. China.
Feng PanDepartment of Orthopedics, Guizhou Provincial Orthopedics Hospital, Guiyang, Guizhou 550000, P.R. China.
Bing QiuDepartment of Orthopedics, Guizhou Provincial Orthopedics Hospital, Guiyang, Guizhou 550000, P.R. China.
Bensen TangDepartment of Orthopedics, Guizhou Provincial Orthopedics Hospital, Guiyang, Guizhou 550000, P.R. China.
Guizhou Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Keratins are fibrous structural proteins that serve essential roles in forming the stratum corneum and protect the cells in this layer of skin from damage. Keratin 17 (KRT17) is a key member of the keratins, and dysregulated expression of KRT17 has been reported in various types of cancer, such as lung and gastric cancer. The present study aimed to identify the role of KRT17 in osteosarcoma and the underlying molecular mechanism. The expression of KRT17 in osteosarcoma tissues and cell lines was detected using reverse transcription‑quantitative PCR (RT‑qPCR) and western blotting. The effects of KRT17 on osteosarcoma cell proliferation and the Warburg effect in vitro were detected using CCK‑8 and colony formation assays, cell cycle distribution analysis and metabolic measures. The effects of KRT17 on osteosarcoma cell proliferation in vivo were detected using a subcutaneous tumorigenesis model. The association between KRT17 and the AKT/mTOR/hypoxia‑inducible factor 1α (HIF1α) pathway was detected using RT‑qPCR and western blotting. The results demonstrated that KRT17 was highly expressed in osteosarcoma tissues and cell lines. Knockdown of KRT17 decreased osteosarcoma cell proliferation and colony formation, induced G1 phase arrest and inhibited glycolysis in vitro. Similarly, the suppression of KRT17 decreased osteosarcoma tumor growth in vivo. Knockdown of KRT17 decreased the expression of phosphorylated (p)‑AKT, p‑mTOR, HIF1α and the target gene of HIF1α glucose transporter 1. Restoring the expression of p‑AKT, p‑mTOR or HIF1α reversed the effect of KRT17 inhibition on cell proliferation and glycolysis. These results indicated that knockdown of KRT17 may be an effective method for treating osteosarcoma through inhibiting osteosarcoma cell proliferation and the Warburg effect by suppressing the AKT/mTOR/HIF1α pathway.

Indexed as

Up-RegulationWarburg Effect, OncologicAdolescentAdultAnimalsBone NeoplasmsCell Line, TumorCell ProliferationChildFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansHypoxia-Inducible Factor 1, alpha SubunitKeratin-17MaleHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitKeratin-17KRT17 protein, humanMTOR protein, humanProto-Oncogene Proteins c-aktRNA, Small InterferingTOR Serine-Threonine KinasesAKT/mTOR/hypoxia‑inducible factor 1αkeratin 17osteosarcomaproliferationWarburg effect

Identifiers

PMID32627037
PMCPMC7251737
OpenAlexW3024944180

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.