Tu1680 Junctional Adhesion Molecule-a Is a Contributing Factor for Gastric Cancer Cell Proliferation and Invasion

Ikeo, Koichi; Oshima, Tadayuki; Shan, Jing; Nagano, Yumiko; Matsui, Hirofumi; Yamasaki, Takahisa; Tomita, Toshihiko; Fukui, Hirokazu; Watari, Jiro; Miwa, Hiroto

doi:10.1016/s0016-5085(14)62956-5

Cited by 1 publication

(1 citation statement)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We first identified that JAM-A was upregulated in multiple cancers, especially BRCA, CHOL, COAD, GBM, OV, PAAD, READ, STAD, TGCT, UCEC, and UCS, and overexpression was shown to be related to poor overall survival and a significant risk factor in BRCA, GBMLGG, and PAAD. The results were generally consistent with previous reports [29,[39][40][41][42][43]. However, there is research on which low levels of JAM-A are associated with worse survival, as assessed by retrospective immunohistochemistry in pancreatic cancer [44].…”

Section: Discussionsupporting

confidence: 91%

Identification and Validation of JAM-A as a Novel Prognostic and Immune Factor in Human Tumors

Ren,

Zheng,

Liu

et al. 2024

Biomedicines

View full text Add to dashboard Cite

Junctional adhesion molecule-A (JAM-A), also known as F11 receptor (F11R), is a transmembrane glycoprotein that is involved in various biological processes, including cancer initiation and progression. However, the functional characteristics and significance of JAM-A in pan-cancer remain unexplored. In this study, we used multiple databases to gain a comprehensive understanding of JAM-A in human cancers. JAM-A was widely expressed in various tissues, mainly located on the microtubules and cell junctions. Aberrant expression of JAM-A was detected in multiple cancers at both mRNA and protein levels, which can be correlated with poorer prognosis and may be attributed to genetic alterations and down-regulated DNA methylation. JAM-A expression was also associated with immune infiltration and may affect immunotherapy responses in several cancers. Functional enrichment analysis indicated that JAM-A participated in tight junction and cancer-related pathways. In vitro experiments verified that JAM-A knockdown suppressed the proliferation and migration abilities of breast cancer cells and liver cancer cells. Overall, our study suggests that JAM-A is a pan-cancer regulator and a potential biomarker for predicting prognosis and immune-therapeutic responses for different tumors.

show abstract