The present study investigated the association between the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway with tumor progression and prognosis of colon cancer. A total of 62 patients with colon cancer were selected as the colon cancer group, and 40 patients with colon lesions were selected as the benign colon lesion group. Immunohistochemistry was used to detect the expression levels of JAK-1 and STAT-3 proteins in colon tissues. The association of JAK-1 and STAT-3 proteins with the pathological parameters and prognosis of colon cancer were analyzed. The total positive rates of JAK-1 and STAT-3 proteins in lesions of patients in the colon cancer group were significantly higher compared with those in the benign colon lesion group (P<0.05). The positive expression of JAK-1 and STAT-3 proteins in patients with colon cancer were not significantly associated with sex, age, tumor differentiation degree and neurovascular invasion (P>0.05), but significantly associated with the clinical stage of colon cancer, tumor infiltration depth and lymph node metastasis (P<0.05). The survival time of patients with colon cancer with positively-expressed JAK-1 and STAT-3 proteins was significantly shorter compared with that of patients with negatively-expressed JAK-1 and STAT-3 proteins (P<0.05). tumor-node-metastasis (TNM) stage, lymph node metastasis and the expression of JAK-1 and STAT-3 proteins in the tumor were associated with the prognosis of patients with colon cancer (P<0.05). TNM stage and the expression levels of JAK-1 and STAT-3 proteins were independent risk factors influencing the prognosis of colon cancer (P<0.05). The JAK/STAT signal may be used as a novel tumor marker and prognostic factor for the diagnosis, assessment and prognosis of colon cancer.
Combination chemotherapy with POFL offers a new, active and safe approach to the treatment of recurrent or metastatic gastric cancer.
Molecular heterogeneity determines the differences in the pathological features, prognosis and survival after relapse when comparing left-sided colon cancer (LCC) and right-sided colon cancer (RCC). At present, the discrepancy in the underlying molecular events between the two types of colon cancer has not been thoroughly investigated. The present study aimed to explore novel targets to predict the disease stage and prognosis of LCC and RCC. Expression analysis of guanine nucleotide binding-protein γ subunit 4 (GNG4) was performed using the Gene Expression Profiling Interactive Analysis (GEPIA) and Oncomine databases. Survival and association analyses were performed using GEPIA and the colon adenocarcinoma dataset from The Cancer Genome Atlas database. GNG4-positive cells in a tissue microarray were examined using immunohistochemistry. According to the GNG4 expression data from Caucasian patients included in the TCGA dataset, GNG4 was highly expressed and positively associated with pathological stage and overall survival (OS) rates in colon cancer. GNG4 expression was higher in LCC than in RCC. Patients with LCC with high GNG4 expression exhibited higher pathological stage and lower survival rates, whereas this was not observed in patients with RCC. In addition, the clinical tissues used in the microarray showed that GNG4 expression was increased in Chinese patients with LCC compared with that in patients with RCC. Consistently, GNG4 expression was negatively associated with OS in patients with LCC, but not in patients with RCC. However, no association was observed between GNG4 expression and the disease stage of colon cancer in both patients with LCC and RCC. Overall, the molecular heterogeneity of GNG4 in LCC and RCC suggests that GNG4 may be used as a diagnostic and prognostic biomarker in patients with LCC.
Background: Long non-coding RNA (lncRNA) LINC01569 plays an important role in regulating the tumor microenvironment (TME) and macrophage polarization. However, whether it participates in the progression of hypopharyngeal carcinoma by regulating the TME remains unclear. Methods: An online database was used to analyze clinical data. Macrophage polarization was detected using qRT-PCR and flow cytometry. In vivo experiments were performed using tumor-bearing nude mice. A co-culture system of hypopharyngeal carcinoma cells and macrophages was used to explore the interactions between the two cell types. Results: LINC01569 enhancement was observed in hypopharyngeal carcinoma tumor-associated macrophages (TAMs). In IL4-induced M2 macrophages, the expression of LINC01569 increased, while LINC01569 expression declined significantly in LPS-induced M1 macrophages. SiRNA-mediated downregulation of LINC01569 inhibits IL4-induced M2 macrophage polarization. Using online databases and a dual-luciferase reporter, miR-193a-5p was confirmed as a potential downstream sponge of LINC01569. MiR-193a-5p expression decreased in IL4-mediated M2 macrophages, which was restored by LINC01569 downregulation. Additionally, LINC01569 inhibition-mediated blocking of M2 macrophage polarization was moderately abolished by transfection with the miR-193a-5p inhibitor. Fatty acid desaturase 1 (FADS1) was verified as a downstream target of miR-193a-5p, and LINC01569 downregulation-mediated inhibition of FADS1 was blocked by miR-193a-5p mimics. Importantly, LINC01569 downregulation-mediated decline in M2 macrophage polarization was abolished by miR-193a-5p mimics, which was further reversed by FADS1 knockdown. Implantation of a mixture of FaDu cells and IL4-induced macrophages promoted tumor growth and proliferation, which were abrogated by the knockdown of LINC01569 in macrophages. Using an in co-culture system of FaDu cells and macrophages in vitro , M2 macrophage-regulated cell growth and apoptosis of FaDu cells were found to be mediated by the LINC01569/miR-193a-5p signaling axis. Conclusion: LINC01569 is highly expressed in the TAMs of hypopharyngeal carcinoma. LINC01569 downregulation restrains macrophages from polarizing toward M2 through the miR-193a-5p/FADS1 signaling axis, thereby helping tumor cells escape inherent immune surveillance and promoting the occurrence and development of hypopharyngeal carcinoma.
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