Journal
ONCOTARGET
Volume 8, Issue 2, Pages 3132-3143Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.13624
Keywords
CD147; non-canonical NF kappa B; apoptosis; spermatocytes; spermatogenesis
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Funding
- National 973 Projects [2013CB967401, 2013CB967404]
- National Science Foundation of China [81671432, 31071019, 31140034]
- Science and Technology Planning Project of Guangdong Province [2016A020218005]
- Fund for high level medical discipline construction of Shenzhen [2016031638]
- Focused Investment Scheme of the Chinese University of Hong Kong
- Hong Kong University Grants Committee [GRF/CUHK/466413]
- Hong Kong PhD Fellowship Scheme (HKPFS) - RGC of Hong Kong
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CD147 null mutant male mice are infertile with arrested spermatogenesis and increased apoptotic germ cells. Our previous studies have shown that CD147 prevents apoptosis in mouse spermatocytes but not spermatogonia. However, the underlying mechanism remains elusive. In the present study, we aim to determine the CD147-regulated apoptotic pathway in mouse spermatocytes. Our results showed that immunodepletion of CD147 triggered apoptosis through extrinsic apoptotic pathway in mouse testis and spermatocyte cell line (GC-2 cells), accompanied by activation of non-canonical NF kappa B signaling and suppression of canonical NF kappa B signaling. Furthermore, CD147 was found to interact with TRAF2, a factor known to regulate NF kappa B and extrinsic apoptotic signaling, and interfering CD147 led to the decrease of TRAF2. Consistently, depletion of CD147 by CRISPR/Cas9 technique in GC-2 cells down-regulated TRAF2 and resulted in cell death with suppressed canonical NF kappa B and activated non-canonical NF kappa B signaling. On the contrary, interfering of CD147 had no effect on NF kappa B signaling pathways as well as TRAF2 protein level in mouse spermatogonia cell line (GC-1 cells). Taken together, these results suggested that CD147 plays a key role in reducing extrinsic apoptosis in spermatocytes, but not spermatogonia, through modulating NF kappa B signaling pathway.
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