<p>Roles Of EAAT1, DHFR, And Fetuin-A In The Pathogenesis, Progression And Prognosis Of Chondrosarcoma</p>

Abstract

AimsChondrosarcoma (CS) is a high-morbidity, relatively common bone malignancy without well-established biomarkers. The proteins EAAT1, DHFR, and fetuin-A have been investigated in many cancers, but their specific relationship to CS has not been reported. The present study examined EAAT1, DHFR, and fetuin-A expression in CS and the clinicopathological significance of these proteins in CS pathogenesis, progression, and prognosis.MethodsEAAT1, DHFR, and fetuin-A protein levels in 80 CS and 25 chondroma specimens were measured by immunohistochemistry and related to histological and clinical factors with chi-squared tests. Following univariate survival analysis, ROC curves calculation, and multivariate analysis.ResultsEAAT1, DHFR, and fetuin-A expression levels were significantly higher in the CS group than in the chondroma group (p < 0.05). Their immunopositivity rates were significantly greater in tissues with moderate or poor tumor differentiation, AJCC stage III or IV, Enneking stage II or III, and metastasis (p<0.05 or p<0.01 or p<0.001). Kaplan–Meier survival analysis showed significantly shorter survival in patients with moderately or poorly differentiated tumors, AJCC stage III or IV CS, Enneking stage II or III CS, metastasis, invasion, or EAAT1, DHFR, and fetuin-A immunopositivity (p < 0.05 or p < 0.001). Cox regression analysis showed that moderate or poor tumor differentiation, AJCC stage III or IV, Enneking stage II or III, metastasis, invasion, and EAAT1, DHFR, or fetuin-A immunopositivity correlated negatively with postoperative survival and positively with mortality (p < 0.05). The AUCs for EAAT1, DHFR, and fetuin-A were 0.654 (95% CI: 0.532–0.776, p = 0.025), 0.638 (95% CI: 0.519–0.756, p = 0.039), and 0.670 (95% CI: 0.556–0.784, p = 0.011), respectively.ConclusionEAAT1, DHFR, and fetuin-A may be important biomarkers of the pathogenesis and progression of CS and predictors of its prognosis.

RETRACTED: SLC1A3 promotes gastric cancer progression via the PI3K/AKT signalling pathway

“…Finally, a xenograft tumour growth model showed that SLC1A3 accelerated gastric tumour cell growth in vivo. These results were consistent with previous studies indicating that SLC1A3 is a positive regulator of tumour progression 28‐30 …”

“…Wang et al found that SLC1A3 regulated the self‐renewal capability of tumour stem cells in thyroid cancer 30 . SLC1A3 has also been identified as a potential predictor of patient prognosis in chondrosarcoma 29 . However, the biological role of SLC1A3 in gastric cancer remains unclear.…”

“…High expression of SLC1A3 in glioblastoma is significantly related to poor prognosis, and SLC1A3 can be a new target for immunotherapy without autoimmunity 27,28 . He found that SLC1A3 expression was higher in chondrosarcoma (CS) than in controls, identifying SLC1A3 as a potential biomarker for the pathogenesis and progression of CS 29 . In thyroid cancer, CD133+ cancer cells had a greater capacity for self‐renewal because of their overexpression of SLC1A3 30 .…”

“…27,28 He found that SLC1A3 expression was higher in chondrosarcoma (CS) than in controls, identifying SLC1A3 as a potential biomarker for the pathogenesis and progression of CS. 29 In thyroid cancer, CD133+ cancer cells had a greater capacity for self-renewal because of their overexpression of SLC1A3. 30 However, the role of SLC1A3 in gastric cancer remains unknown.…”

Comprehensive Analysis of Potential Correlation Between Solute Carrier 1A (SLC1A) Family and Lung Adenocarcinoma

“… 8 Sun et al, believed that overexpressed SLC1A3 contributed to L-asparaginase resistance in solid tumors. 45 Previous studies demonstrated that high expression of SLC1A3 in glioblastoma, 46 chondrosarcoma, 47 thyroid cancer. 48 Nevertheless, there was no significant difference in the expression of SLC1A3 between LUAD tissues and control normal tissues in our study.…”