FRA-1 suppresses apoptosis of Helicobacter pylori infected MGC-803 cells

Yang, Yang; You, Benshuai; Dong, Surong; Zhou, Chenglin

doi:10.1007/s11033-020-06105-y

Cited by 3 publications

(3 citation statements)

References 33 publications

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“…As shown in Figure 1B–D , the mRNA and protein levels of Fra‐1 were measured, and the results showed that the expression of Fra‐1 increased over time and peaked 48 h after I/R. Considering that Fra‐1 affects the apoptosis response under some conditions [ 10 , 11 , 12 , 13 , 14 ], we measured the protein expression of cleaved caspase‐3 and found that Fra‐1 and cleaved caspase‐3 were positively correlated, as shown in Figure 1C–F . These data indicated that Fra‐1 may influence the apoptosis response activated by I/R.…”

Section: Resultsmentioning

confidence: 99%

“…Fra‐1 is a member of the Fos family, with members that dimerize with Jun family members [ 4 ], but the function of Fra‐1 after I/R has been unclear. Results from different studies have shown that Fra‐1 has antiapoptotic or proapoptotic functions under different conditions [ 10 , 11 , 12 , 13 , 14 ]. For example, Fra‐1 potentially promotes neuronal apoptosis in rats after traumatic brain injury [ 46 ].…”

Section: Disccussionmentioning

confidence: 99%

“…Some reports have indicated that Fra‐1 controls cell proliferation, survival, and metastasis, but the therapeutic effect of Fra‐1 depends on the cancer cell context [ 9 ]. In addition, Fra‐1 has been shown to suppress apoptosis [ 10 , 11 , 12 ]. However, Fra‐1 has also been reported to promote apoptosis, indicating that the role of Fra‐1 in apoptosis might vary with the type of cell and stimulation [ 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

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Fra‐1 induces apoptosis and neuroinflammation by targeting S100A8 to modulate TLR4 pathways in spinal cord ischemia/reperfusion injury

et al. 2022

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Spinal cord ischemia/reperfusion injury (SCII) is a severe complication driven by apoptosis and neuroinflammation. An increase in the expression of c-Fos, a member of the AP-1 family, is known as a neuronal activation marker in SCII. The AP-1 family is composed of Jun, Fos, and is associated with the regulation of cytokines expression and apoptosis. Fra-1 is a member of the Fos family, however, the contribution of Fra-1 to SCII is still unclear. In our study, Fra-1 was highly upregulated especially in neurons and microglia and promoted apoptosis by changing the expression of Bax/Bcl-2 after SCII. Furthermore, we found that Fra-1 directly regulated the transcription expression of S100A8. We demonstrated that knockdown of Fra-1 alleviated S100A8 mediated neuronal apoptosis and inflammatory factor release, thus improved motor function after SCII. Interestingly, we showed that administration of TAK-242, the TLR4 inhibitor, to the ischemia/ reperfusion (I/R) injury induced rats suppressed the activation of the ERK and NF-κB pathways, and further reduced Fra-1 expression. In conclusion, we found that Fra-1-targeted S100A8 was expressed the upstream of Fra-1, and the Fra-1/S100A8 interaction formed a feedback loop in the signaling pathways activated by SCII.

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