Evidence map›Paper›PMID 37539493›Full record

ArticleJournal of cellular and molecular medicine2023

SPI1 involvement in malignant melanoma pathogenesis by regulation of HK2 through the AKT1/mTOR pathway.

Chunlei Liu, Xiujuan Qiu, Jun Gao, Zhifan Gong, Xiaogang Zhou, Haichao Luo, Xuerui Geng

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-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

8 citing papers in PubMed, 7 citations in OpenAlex.

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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 1 institution in 1 country.

Chunlei LiuDepartment of dermatology, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, China.
Xiujuan QiuDepartment of oncology, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, China.
Jun GaoDepartment of general surgury, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, China.
Zhifan GongDepartment of dermatology, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, China.
Xiaogang ZhouDepartment of dermatology, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, China.
Haichao LuoDepartment of oncology, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, China.
Xuerui GengDepartment of dermatology, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, China.ORCID 0000-0002-4591-9235
Hubei University of Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spi-1 proto-oncogene (SPI1) plays a vital role in carcinogenesis. Our work aimed to investigate the potential regulatory mechanism of SPI1 in melanoma. The mRNA and protein levels were measured via qRT-PCR and Western blotting. Cell viability was assessed by CCK-8 assay. The target relationship between SPI1 and hexokinase 2 (HK2) was determined using dual-luciferase reporter detection. ChIP was conducted to confirm the targeted relationship between SPI1 and the HK2 promoter. Immunohistochemistry analysis was conducted to measure the positive cell number of SPI1 and HK2 in melanoma tissues. The cell migration abilities were determined using a wound healing assay. Glucose consumption, pyruvate dehydrogenase activity, lactate production and ATP levels were measured to assess glycolysis. SPI1 transcription in melanoma cells and tissues was dramatically higher than that in adjacent normal tissues and epidermal melanocyte HEMa-LP, respectively. Knockdown of SPI1 restrained cell viability, metastasis and glycolysis in melanoma cells. SPI1 directly targeted HK2, and knockdown of SPI1 repressed HK2 expression. Overexpression of HK2 weakened the inhibitory effects of SPI1 knockdown on the viability, metastasis and glycolysis of melanoma cells. The serine-threonine kinase 1 (AKT1)/mammalian target of rapamycin (mTOR) axis is involved in melanoma progression. SPI1 knockdown restrained melanoma cell proliferation, metastasis and glycolysis by regulating the AKT1/mTOR pathway.

Indexed as

MelanomaMicroRNAsCell Line, TumorCell ProliferationCutaneous Malignant MelanomaHexokinaseHumansProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAKT1 protein, humanHexokinaseMicroRNAsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAKT1/mTOR pathwayglycolysishexokinase 2 (HK2)melanomaSPI-1 proto-oncogene (SPI1)

Identifiers

PMID37539493
PMCPMC10494286
OpenAlexW4385564043

What OpenQuestion holds

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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.