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Gao Fuxian,Wang Chunxiao,Ji Jianghai,Li Wenjuan 대한독성 유전단백체 학회 2023 Molecular & cellular toxicology Vol.19 No.3
Background Cervix cancer (CC) is the most common gynecological malignancy and the leading cause of morbidity in women around the world. Objectives In this research, the eff ect of FBXO22 on HPV-associated CC was evaluated. Results The results fi rst illuminated that FBXO22 was highly expressed in HPV + CC patients. FBXO22 knockdown inhibited the proliferation of HPV + CC cells, and promoted autophagy in HPV + CC cells. Finally, FBXO22 regulates the LKB1/ AMPK pathway . Conclusion This research hinted that FBXO22 promotes cell proliferation and inhibits autophagy in HPV-associated CC by inactivating the LKB1/AMPK pathway.
Zhao Chijun,Jia Xinglin,Pan Yanying,Liao Simeng,Zhang Shuo,Ji Chunxiao,Kuang Guangwei,Wu Xin,Liu Quan,Tang Yulong,Fang Lihua 한국미생물학회 2023 The journal of microbiology Vol.61 No.4
Streptococcus suis serotype 2 (SS2) is an important zoonotic pathogen that can infect humans in contact with infected pigs or their byproducts. It can employ different types of genes to defend against oxidative stress and ensure its survival. The thioredoxin (Trx) system is a key antioxidant system that contributes adversity adaptation and pathogenicity. SS2 has been shown to encode putative thioredoxin genes, but the biological roles, coding sequence, and underlying mechanisms remains uncharacterized. Here, we demonstrated that SSU05_0237-ORF, from a clinical SS2 strain, ZJ081101, encodes a protein of 104 amino acids with a canonical CGPC active motif and an identity 70–85% similar to the thioredoxin A (TrxA) in other microorganisms. Recombinant TrxA efficiently catalyzed the thiol-disulfide oxidoreduction of insulin. The deletion of TrxA led to a significantly slow growth and markedly compromised tolerance of the pathogen to temperature stress, as well as impaired adhesion ability to pig intestinal epithelial cells (IPEC-J2). However, it was not involved in H2O2 and paraquat-induced oxidative stress. Compared with the wild-type strain, the ΔTrxA strain was more susceptible to killing by macrophages through increasing NO production. Treatment with TrxA mutant strain also significantly attenuated cytotoxic effects on RAW 264.7 cells by inhibiting inflammatory response and apoptosis. Knockdown of pentraxin 3 in RAW 264.7 cells was more vulnerable to phagocytic activity, and TrxA promoted SS2 survival in phagocytic cells depending on pentraxin 3 activity compared with the wild-type strain. Moreover, a co-inoculation experiment in mice revealed that TrxA mutant strain is far more easily cleared from the body than the wild type strain in the period from 8–24 h, and exhibits significantly attenuated oxidative stress and liver injury. In summary, we reveal the important role of TrxA in the pathogenesis of SS2.