Objectives Though carotid body tumors are rare, increasing attentions have been given because of malignant transformation and high surgical risk. However, at present, the characteristics and etiology still remain unclear. Our study was designed to describe the clinical features of carotid body tumors in our institution and to compare the results with previous reports. Methods We retrospectively reviewed carotid body tumor patients diagnosed in our institution from January 2015 to May 2020. The demographics, comorbidities, lesion location, anatomic characteristics, complications, and postoperative outcomes were evaluated. Carotid body tumor measurements were determined from computed tomography, magnetic resonance imaging, and carotid arteriography examination. We described and compared the clinical features of carotid body tumors in our institution and other reports. Results We totally identified 122 carotid body tumor cases for the present analysis. The mean age was 50.26 years, with the majority being female (82%). The commonest presentation was a painless neck mass (68%). For the distribution of nationality, most patients were the Han nationality (69.7%). The mean altitude of habitat of patients was 2689.4 km; 19.7% patients suffered bilateral lesions. The main blood supply of carotid body tumors was from external carotid artery (54.1%). For patients who received operation, 11 (11.2%) patients experienced cranial nerve injury. The maximal diameter of tumors was 3.99 ± 1.98 cm in male and 3.38 ± 1.36 cm in female. The volume of tumors was 31.49 ± 29.76 cm3 in male and 15.27 ± 13.06 cm3 in female. The distance to base of skull of tumors was 3.39 ± 1.07 cm (3.99 ± 1.98 cm in male vs 3.38 ± 1.36 cm, P <  0.05). Two patients (2.04%) were identified as having malignant carotid body tumor. Conclusions Though carotid body tumor had a low morbidity and multitudinous clinicopathologic features, it was apt to middle-aged women and the main blood supply was from external carotid artery. The painless neck mass was the commonest presentation of carotid body tumors. There were significant difference between male and female patients regarding platelet, hemoglobin, distance to base of skull, tumor volume, altitude of habitat, carotid body tumor location, and hypertension.

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Overexpressed gastrin is reported to promote oncogenesis and development of gastric cancer by inhibiting apoptosis of cancer cells; however, the underlying mechanism remains unclear. Our study is aimed at revealing the mechanism underlying the effect of gastrin on apoptosis of gastric cancer cells. Gastrin-interfering cell line was constructed by stably transfecting gastrin-specific pshRNA plasmid to gastric cancer cell line BGC-823. Then, differentially expressed proteins between untreated BGC-823 and gastrin-interfering BGC-823 cell lines were detected by the iTRAQ technique. GO and KEGG analysis was used to analyze the differentially expressed genes that code these differentially expressed proteins. The Annexin V-FITC staining assay was used to detect gastric cancer cell apoptosis. The DCFH-DA fluorescent probe staining assay was used to measure intracellular ROS. Mitochondrial membrane potential was detected by flow cytometry. Western blot was used to analyze the mitochondria respiratory chain proteins and apoptosis-related proteins. A total of 107 differentially expressed proteins were identified by iTRAQ. GO and KEGG analysis showed that proteins coded by the corresponding differentially expressed genes were mainly enriched in the mitochondrial oxidative respiratory chain, and the expression of three proteins (COX17, COX5B, ATP5J) was upregulated. The three proteins with higher scores were verified by Western blot. The apoptosis rate of the gastrin knockdown cancer cell was significantly increased; meanwhile, gastrin knockdown leads to increase of membrane potential and decrease of intracellular ROS production. Additionally, Bax was significantly increased, whereas NF-κB-p65 and Bcl-2 were downregulated after knockdown of gastrin. Concomitantly, pretreatment with NAC reversed the effect of gastrin on the Bax and Bcl-2 expression. Gastrin promotes the production of ROS from mitochondria, activates NF-κB, and inhibits apoptosis via modulating the expression level of Bcl-2 and Bax.

Gastrin plays a vital role in the development and progression of gastric cancer (GC). Its expression is up-regulated in GC tissues and several GC cell lines. Yet, the underlying mechanism remains to be investigated. Here, we aim to investigate the role and mechanism of gastrin in GC proliferation. Gastrin-overexpressing GC cell model was constructed using SGC7901 cells. Then the differentially expressed proteins were identified by iTRAQ analysis. Next, we use flow cytometry and immunofluorescence to study the effect of gastrin on the mitochondrial potential and mitochondria-derived ROS production. Finally, we studied the underlying mechanism of gastrin regulating mitochondrial function using Co-IP, mass spectrometry and immunofluorescence. Overexpression of gastrin promoted GC cell proliferation in vitro and in vivo. A total of 173 proteins were expressed differently between the controls and gastrinoverexpression cells and most of these proteins were involved in tumorigenesis and cell proliferation. Among them, Cox17, Cox5B and ATP5J that were all localized to the mitochondrial respiratory chain were down-regulated in gastrin-overexpression cells. Furthermore, gastrin overexpression led to mitochondrial potential decrease and mitochondria-derived ROS increase. Additionally, gastrin-induced ROS generation resulted in the inhibition of cell apoptosis via activating NF-κB, inhibiting Bax expression and promoting Bcl-2 expression. Finally, we found gastrin interacted with mitochondrial membrane protein Annexin A2 using Co-IP and mass spectrometry. Overexpr ession of gastrin inhibits GC cell apoptosis by inducing mitochondrial dysfunction through interacting with mitochondrial protein Annexin A2, then up-regulating ROS production to activate NF-κB and further leading to Bax/Bcl-2 ratio decrease.