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

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 betw...

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Autores principales: Liu, Chunlei, Qiu, Xiujuan, Gao, Jun, Gong, Zhifan, Zhou, Xiaogang, Luo, Haichao, Geng, Xuerui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10494286/
https://www.ncbi.nlm.nih.gov/pubmed/37539493
http://dx.doi.org/10.1111/jcmm.17844
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author Liu, Chunlei
Qiu, Xiujuan
Gao, Jun
Gong, Zhifan
Zhou, Xiaogang
Luo, Haichao
Geng, Xuerui
author_facet Liu, Chunlei
Qiu, Xiujuan
Gao, Jun
Gong, Zhifan
Zhou, Xiaogang
Luo, Haichao
Geng, Xuerui
author_sort Liu, Chunlei
collection PubMed
description 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.
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spelling pubmed-104942862023-09-12 SPI1 involvement in malignant melanoma pathogenesis by regulation of HK2 through the AKT1/mTOR pathway Liu, Chunlei Qiu, Xiujuan Gao, Jun Gong, Zhifan Zhou, Xiaogang Luo, Haichao Geng, Xuerui J Cell Mol Med Original Articles 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. John Wiley and Sons Inc. 2023-08-04 /pmc/articles/PMC10494286/ /pubmed/37539493 http://dx.doi.org/10.1111/jcmm.17844 Text en © 2023 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Liu, Chunlei
Qiu, Xiujuan
Gao, Jun
Gong, Zhifan
Zhou, Xiaogang
Luo, Haichao
Geng, Xuerui
SPI1 involvement in malignant melanoma pathogenesis by regulation of HK2 through the AKT1/mTOR pathway
title SPI1 involvement in malignant melanoma pathogenesis by regulation of HK2 through the AKT1/mTOR pathway
title_full SPI1 involvement in malignant melanoma pathogenesis by regulation of HK2 through the AKT1/mTOR pathway
title_fullStr SPI1 involvement in malignant melanoma pathogenesis by regulation of HK2 through the AKT1/mTOR pathway
title_full_unstemmed SPI1 involvement in malignant melanoma pathogenesis by regulation of HK2 through the AKT1/mTOR pathway
title_short SPI1 involvement in malignant melanoma pathogenesis by regulation of HK2 through the AKT1/mTOR pathway
title_sort spi1 involvement in malignant melanoma pathogenesis by regulation of hk2 through the akt1/mtor pathway
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10494286/
https://www.ncbi.nlm.nih.gov/pubmed/37539493
http://dx.doi.org/10.1111/jcmm.17844
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