Expression of tripartite motif-containing 44 and its prognostic and clinicopathological values in human malignancies: a meta-analysis

Xiao, Guoliang; Yang, Qiuxi; Bao, Ziwei; Mao, Haixia; Zhang, Yi; Lin, Shibu

doi:10.21203/rs.3.rs-15897/v1

Cited by 1 publication

(1 citation statement)

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“…Previous studies related to TRIM44 are mainly on cancer. TRIM44 is elevated in various cancer types, and high TRIM44 levels are associated with poor survival of patients with cancer and a higher recurrence rate [25]. TRIM44 overexpression increases tumor cell proliferation, migration, and survival, while suppression of TRIM44 expression inhibits cancer cell proliferation and invasion [26, 27].…”

Section: Discussionmentioning

confidence: 99%

Silencing of TRIM44 Inhibits Inflammation and Alleviates Traumatic Brain Injury in Rats by Downregulating TLR4-NF-κB Signaling

Zhu¹,

Dong²,

Yue³

et al. 2022

Neuroimmunomodulation

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Background: Neuroinflammation subsequent to traumatic brain injury (TBI) is important for the recovery of patients and is associated with neurodegenerative changes post-TBI. The tripartite motif containing 44 (TRIM44) protein is an E3 ligase involved in the regulation of immune function with no previously known link to TBI. This study explores the connection between TRIM44 and TBI. Methods: After induction of TBI in rats by control cortex injury, TRIM44 expressions were determined with quantitative real-time reverse transcription polymerase chain reaction and Western blot, and Toll-like receptor 4 (TLR4)-NF-κB signaling was examined by the expression of TLR4, p65 phosphorylation, and the specific NF-κB transcription activity. The effects of TRIM44 knockdown on inflammation, neurological function, and TLR4-NF-κB signaling in TBI rats were revealed by the detection of proinflammatory cytokines and TLR4-NF-κB signaling molecules, modified neurological severity score, brain water content, and Evans blue permeability. Results: We found that TRIM44 expression was significantly increased following TBI induction along with TLR4-NF-κB activation. Silencing of TRIM44 suppressed proinflammatory cytokine production, improved neurological outcomes, alleviated brain edema, and inhibited TLR4-NF-κB signaling in TBI rats. Conclusion: Our findings suggest that suppressing TRIM44 or modulation of relevant pathways may be a therapeutic strategy for TBI.

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Section: Discussionmentioning

confidence: 99%