Int J Med Sci
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Objective: Evaluate the prognostic value of monocyte-lymphocyte ratio (MLR) in patients with stage I endometrial cancer. Method: Data from 225 patients with stage I endometrioid endometrial cancer who underwent surgical resection between January 2010 and December 2020 were reviewed. The receiver operating characteristic (ROC) curves were generated for the neutrophil-lymphocyte ratio, platelet-lymphocyte ratio, and MLR. ⋯ In multivariate analysis, grade, depth of myometrial invasion, adjuvant RT, and high MLR were independent prognostic factors for disease-free survival. Conclusion: Elevated MLR was significantly associated poor clinical outcomes in patients with stage I endometrioid endometrial cancer. Our findings suggest that MLR may be clinically reliable and useful as an independent prognostic marker for patients with stage I endometrioid endometrial cancer.
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Oral cancer is the eighth greatest generally diagnosed cancer amongst males worldwide and the fourth most generally malignancy amongst Taiwanese males. The pro-inflammatory adipocytokine visfatin promotes tumor growth. Elevated plasma visfatin levels have been identified in patients with oral squamous cell carcinoma (OSCC), although the biological mechanisms underlying the involvement of visfatin in the pathogenesis of OSCC are not well understood. ⋯ We also examined the associations between these visfatin genotypes and OSCC histopathological prognostic factors (pathological stage, tumor status, lymph node status, and metastasis). We found that compared with subjects with the CC genotype of SNP rs11977021, those with the CT+TT genotype were less likely to progress OSCC. In addition, an association was found between the rs4730153 variant and lymph node metastasis in the OSCC cohort.
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Esophageal squamous cell carcinoma (ESCC) is notorious for the rapid progression especially early tumor metastasis due to the unclear mechanism. Recently, ETV5 attracts much attention for its potential role as an oncogenic transcription factor involved in multiple cancers. However, no one reported the mechanism behind the association between ETV5 expression and esophageal squamous cell carcinoma progression. ⋯ In conclusion, ETV5 was associated with ESCC tumor staging and ESCC prognosis clinically. ETV5 promoted metastasis of ESCC by activating MMPs through augmenting the transcription of SKA1 and TRPV2. ETV5 was likely to be a novel oncogene and therapeutic target in ESCC.
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Purpose: We aimed to evaluate whether CEMIP plays any role in the survival outcome of breast cancer (BC) patients, as well as to explore the regulatory mechanism of CEMIP in BC. Methods: We evaluated the expression and prognostic effect of CEMIP in BC patients using the Oncomine, GEPIA, UALCAN, and Kaplan-Meier plotter databases. Additionally, we detected CEMIP mRNA and protein levels in BC and normal tissues via PCR and western blotting analyses. ⋯ CEMIP expression was associated with an adverse prognosis. CEMIP and its coexpressed genes can participate in the progression of BC. Therefore, CEMIP may be a potential biomarker for the treatment of BC patients.
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Gastric cancer is a highly malignant tumor. Gastric cancer stem cells (GCSCs) are the main causes of drug resistance, metastasis, recurrence, and poor prognosis. As a secondary metabolite of lichen, Atranorin has a variety of biological effects, such as antibacterial, anti-inflammatory, analgesic, and wound healing; however, its killing effect on GCSCs has not been reported. ⋯ The results of high performance liquid chromatography-mass spectrometry and Dot blotting showed that Atranorin@SPION significantly inhibited the mRNA 5‑hydroxymethylcytidine modification of GCSCs. Meanwhile, the results of RNA immunoprecipitation-PCR also indicated that Atranorin@SPIONs significantly reduced the 5-hydroxymethylcytidine modification level of GPX4 and SLC7A11 mRNA 3' untranslated region in GCSCs, resulting in a decrease in their stability, shortening their half-lives and reducing translation activity. Therefore, this study revealed that Atranorin@SPIONs induced ferroptosis of GCSCs by weakening the expression of the Xc-/GPX4 axis and the 5-hydroxymethylcytidine modification of mRNAs in the pathway, thereby achieving their therapeutic effect on gastric cancer.