Knockdown of FUT11 inhibits the progression of gastric cancer via the PI3K/AKT pathway
Gastric cancer (GC) is a common and highly malignant tumor of the digestive tract. Members of the focused fucosyltransferase (FUT) family participate in the advancement of various types of cancer. However, research of FUT family members in the progression of GC known to be limited. The purpose of th...
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Elsevier
2023-07-01
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author | Wenpeng Cao Zhirui Zeng Jinzhi Lan Yushi Yang Min Lu Shan Lei |
author_facet | Wenpeng Cao Zhirui Zeng Jinzhi Lan Yushi Yang Min Lu Shan Lei |
author_sort | Wenpeng Cao |
collection | DOAJ |
description | Gastric cancer (GC) is a common and highly malignant tumor of the digestive tract. Members of the focused fucosyltransferase (FUT) family participate in the advancement of various types of cancer. However, research of FUT family members in the progression of GC known to be limited. The purpose of the research was to determine the function of important affiliates of the FUT family in GC and to explore its impacts on the proliferation and migration of GC cells and molecular mechanisms. For the study, fucosyltransferase11 (FUT11) was confirmed to be the only affiliate of the FUT family that was upmodulated in GC tissues and linked to poor survival according to GEPIA data. Furthermore, compared with adjacent noncancerous tissues, the expression of FUT11 was increased in GC tissues. The elevated FUT11 expression suggested that the overall survival (OS) rate of GC is low. Inhibition of FUT11 significantly reduced the proliferation and migration and suppressed the PI3K/AKT pathway by down-regulated collagen type VI alpha 3 chain (COL6A3) in GC cells. The present study has demonstrated that reinstating the expression of COL6A3 in gastric cancer (GC) cells can counteract the inhibitory impact of FUT11 knockdown on the proliferation and migration of GC cells. In conclusion, FUT11 may serve as a novel biomarker for GC, as it modulates GC cell proliferation and migration through the PI3K/AKT signaling pathway. |
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institution | Directory Open Access Journal |
issn | 2405-8440 |
language | English |
last_indexed | 2024-03-12T21:38:08Z |
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spelling | doaj.art-1631bfc2dd7342a8a79946b6cb2827f22023-07-27T05:56:48ZengElsevierHeliyon2405-84402023-07-0197e17600Knockdown of FUT11 inhibits the progression of gastric cancer via the PI3K/AKT pathwayWenpeng Cao0Zhirui Zeng1Jinzhi Lan2Yushi Yang3Min Lu4Shan Lei5Department of Anatomy, School of Basic Medicine, Guizhou Medical University, Guiyang 550009, Guizhou, ChinaDepartment of Physiology, School of Basic Medicine, Guizhou Medical University, Guiyang 550009, Guizhou, ChinaDepartment of Physiology, School of Basic Medicine, Guizhou Medical University, Guiyang 550009, Guizhou, ChinaDepartment of Pathology, Affiliated Hospital of Guizhou Medical University, Guiyang 550009, Guizhou, ChinaDepartment of Gastroenterology, Zhujiang Hospital, Southern Medical University, Guangzhou, 510000, Guangdong, China; Corresponding author. Zhujiang Hospital, Southern Medical University, Guangzhou, 510000, Guangdong, China.Department of Physiology, School of Basic Medicine, Guizhou Medical University, Guiyang 550009, Guizhou, China; Corresponding author. School of Basic Medicine, Guizhou Medical University, Dongqing Road, Guiyang, Guizhou 550009, PR China.Gastric cancer (GC) is a common and highly malignant tumor of the digestive tract. Members of the focused fucosyltransferase (FUT) family participate in the advancement of various types of cancer. However, research of FUT family members in the progression of GC known to be limited. The purpose of the research was to determine the function of important affiliates of the FUT family in GC and to explore its impacts on the proliferation and migration of GC cells and molecular mechanisms. For the study, fucosyltransferase11 (FUT11) was confirmed to be the only affiliate of the FUT family that was upmodulated in GC tissues and linked to poor survival according to GEPIA data. Furthermore, compared with adjacent noncancerous tissues, the expression of FUT11 was increased in GC tissues. The elevated FUT11 expression suggested that the overall survival (OS) rate of GC is low. Inhibition of FUT11 significantly reduced the proliferation and migration and suppressed the PI3K/AKT pathway by down-regulated collagen type VI alpha 3 chain (COL6A3) in GC cells. The present study has demonstrated that reinstating the expression of COL6A3 in gastric cancer (GC) cells can counteract the inhibitory impact of FUT11 knockdown on the proliferation and migration of GC cells. In conclusion, FUT11 may serve as a novel biomarker for GC, as it modulates GC cell proliferation and migration through the PI3K/AKT signaling pathway.http://www.sciencedirect.com/science/article/pii/S2405844023048089Gastric cancerFucosyltransferase familyFUT11COL6A3Proliferation |
spellingShingle | Wenpeng Cao Zhirui Zeng Jinzhi Lan Yushi Yang Min Lu Shan Lei Knockdown of FUT11 inhibits the progression of gastric cancer via the PI3K/AKT pathway Heliyon Gastric cancer Fucosyltransferase family FUT11 COL6A3 Proliferation |
title | Knockdown of FUT11 inhibits the progression of gastric cancer via the PI3K/AKT pathway |
title_full | Knockdown of FUT11 inhibits the progression of gastric cancer via the PI3K/AKT pathway |
title_fullStr | Knockdown of FUT11 inhibits the progression of gastric cancer via the PI3K/AKT pathway |
title_full_unstemmed | Knockdown of FUT11 inhibits the progression of gastric cancer via the PI3K/AKT pathway |
title_short | Knockdown of FUT11 inhibits the progression of gastric cancer via the PI3K/AKT pathway |
title_sort | knockdown of fut11 inhibits the progression of gastric cancer via the pi3k akt pathway |
topic | Gastric cancer Fucosyltransferase family FUT11 COL6A3 Proliferation |
url | http://www.sciencedirect.com/science/article/pii/S2405844023048089 |
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