ArticleFrontiers in oncology2026
Silencing TMED2 suppresses cell growth and tumor progression in diffuse large B-cell lymphoma via inducing G0/G1 cell cycle arrest.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Transmembrane Emp24 Domain Containing 2 (TMED2) is involved in various cancers, but its role in diffuse large B-cell lymphoma (DLBCL) remains unclear. This study investigated TMED2's expression, biological functions, and underlying mechanisms in DLBCL. Methods: TMED2 expression was analyzed in DLBCL patient samples and cell lines by qRT-PCR and Western blot (WB). Lentiviral shRNA-mediated knockdown of TMED2 was performed in SUDHL-4 and OCI-LY10 DLBCL cells. Functional impacts on proliferation, cell cycle, and apoptosis were assessed using CCK-8, flow cytometry analysis, annexin V-APC staining assays, caspase-3/7 activity assays, and WB of key regulators (cyclins, CDKs, Bax, Bcl-2, caspases). The Results: TMED2 expression was significantly upregulated in DLBCL tissues and cell lines. TMED2 knockdown markedly inhibited cell proliferation Conclusion: TMED2 promotes DLBCL progression by driving cell cycle progression and inhibiting apoptosis. Silencing TMED2 induces G0/G1 arrest and enhances caspase-dependent apoptosis. These findings identify TMED2 as a potential prognostic biomarker and therapeutic target in DLBCL.
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