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SLC6A8 敲低抑制人肝癌 Huh-7 和 Hep3B 细胞的侵袭和迁移。

SLC6A8 Knockdown Suppresses the Invasion and Migration of Human Hepatocellular Carcinoma Huh-7 and Hep3B Cells.

机构信息

Hepatobiliary Surgery, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, China.

出版信息

Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033820983029. doi: 10.1177/1533033820983029.

DOI:10.1177/1533033820983029
PMID:33356959
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7780307/
Abstract

Liver cancer is considered the sixth most commonly diagnosed cancer and the fourth leading cause of cancer-related deaths worldwide. Currently, there is no specific and effective therapy for hepatocellular carcinoma. Therefore, developing novel diagnostic and therapeutic strategies against hepatocellular carcinoma is of paramount importance. Solute carrier family 6 member 8 (SLC6A8) encodes the solute carrier family 6-8 to transport creatine into cells in a Na and Cl- dependent manner. SLC6A8 deficiency is characterized by intellectual disabilities, loss of speech, and behavioral abnormalities. Of concern, the association of SLC6A8 with hepatocellular carcinoma remains elusive. In this study, we revealed that SLC6A8 knockdown significantly induced apoptosis and suppressed the migration and invasion of Hep3B and Huh-7 cells. These findings depicted the vital role of SLC6A8 in the initiation and progression of human hepatocellular carcinoma.

摘要

肝癌被认为是全球第六大常见癌症，也是癌症相关死亡的第四大主要原因。目前，针对肝细胞癌尚无特异性和有效的治疗方法。因此，开发针对肝细胞癌的新型诊断和治疗策略至关重要。溶质载体家族 6 成员 8（SLC6A8）编码溶质载体家族 6-8，以 Na 和 Cl-依赖性方式将肌酸转运到细胞内。SLC6A8 缺陷的特征是智力障碍、丧失语言能力和行为异常。值得关注的是，SLC6A8 与肝细胞癌的关联仍然难以捉摸。在这项研究中，我们揭示了 SLC6A8 敲低显著诱导了 Hep3B 和 Huh-7 细胞的凋亡，并抑制了它们的迁移和侵袭。这些发现描绘了 SLC6A8 在人类肝细胞癌发生和发展中的重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/23002ee76bd5/10.1177_1533033820983029-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/4fb87b76f0dc/10.1177_1533033820983029-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/12ab82a71dc8/10.1177_1533033820983029-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/4e2355c5e544/10.1177_1533033820983029-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/4f2b5c4cb9cd/10.1177_1533033820983029-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/5bc916e86161/10.1177_1533033820983029-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/0638b123f71f/10.1177_1533033820983029-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/23002ee76bd5/10.1177_1533033820983029-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/4fb87b76f0dc/10.1177_1533033820983029-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/12ab82a71dc8/10.1177_1533033820983029-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/4e2355c5e544/10.1177_1533033820983029-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/4f2b5c4cb9cd/10.1177_1533033820983029-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/5bc916e86161/10.1177_1533033820983029-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/0638b123f71f/10.1177_1533033820983029-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d5/7780307/23002ee76bd5/10.1177_1533033820983029-fig7.jpg

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