Search

Dysregulation of microRNA (miRNA) expression in cancer is a significant factor contributing to the progression of chemoresistance. The objective of this study is to explore the underlying mechanisms by which miR-34b-3p regulates chemoresistance in cervical cancer (CC). Previous findings have demonstrated low expression levels of miR-34b-3p in both CC chemoresistant cells and tissues. In this study, we initially characterize the behavior of SiHa/DDP cells which are CC cells resistant to the chemotherapeutic drug cisplatin (DDP). Subsequently, miR-34b-3p mimics are transfected into SiHa/DDP cells. It is observed that overexpression of miR-34b-3p substantially inhibits the proliferation, migration, and invasion abilities of SiHa/DDP cells and also enhances their sensitivity to DDP-induced cell death. Quantitative RT-PCR and western blot analysis further reveal elevated expression levels of STC2 and FN1 in SiHa/DDP cells, contrary to the expression pattern of miR-34b-3p. Moreover, STC2 and FN1 contribute to DDP resistance, proliferation, migration, invasion, and decreased apoptosis in CC cells. Through dual-luciferase assay analysis, we confirm that STC2 and FN1 are direct targets of miR-34b-3p in CC. Finally, rescue experiments demonstrate that overexpression of either STC2 or FN1 can partially reverse the inhibitory effects of miR-34b-3p overexpression on chemoresistance, proliferation, migration and invasion in CC cells. In conclusion, our findings support the role of miR-34b-3p as a tumor suppressor in CC. This study indicates that targeting the miR-34b-3p/STC2 or FN1 axis has potential therapeutic implications for overcoming chemoresistance in CC patients.

Epidemiological studies have shown that air pollution and particulate matter (PM) are closely related to the occurrence of cancer. However, the potential prognostic and immunological biomarkers for air pollution related cancers are lacking. In this study, we proved PM2.5 exposure was correlated with lung cancer through transcriptome analysis. Importantly, we identified STC2 as a key gene regulated by PM2.5, whose expression in epithelial cells was significantly increased after PM2.5 treatment and validated by using RT-qPCR and immunofluorescence. Kaplan-Meier OS curves suggested that high STC2 expression positively correlated with a poor prognosis in lung cancer. Furthermore, we discovered that STC2 was associated with multiple cancers and pathways in cancer. Next, Pan-Cancer Expression Landscape of STC2 showed that STC2 exhibited inconsistent expression across 26 types of human cancer, lower in KIRP in cancer versus adjacent normal tissues, and significantly higher in another cancers. Cox regression results suggested that STC2 expression was positively or negatively associated with prognosis in different cancers. Moreover, STC2 expression was associated with clinical phenotypes including age, gender, stage and grade. Mutation features of STC2 were also analyzed, in which the highest alteration frequency of STC2 was presented in KIRC with amplification. Meanwhile, the effects of copy number variation (CNV) on STC2 expression were investigated across various tumor types, suggesting that STC2 expression was significantly correlated with CNV in tumors. Additionally, STC2 was closely related to tumor heterogeneity, tumor stemness and tumor immune microenvironment like immune cell infiltration. In the meantime, we analyzed methylation modifications and immunological correlation of STC2. The results demonstrated that STC2 expression positively correlated with most RNA methylation genes and immunomodulators across tumors. Taken together, the findings revealed that PM2.5-induced STC2 might be a potential prognostic and immunological biomarker for cancers related to air pollution. [ABSTRACT FROM AUTHOR]

Background & Objective: Colorectal cancer is the third most common cause of cancer death worldwide. Stanniocalcin 2 (STC2) is a glycoprotein hormone over-expressed in many human cancers where it regulates tumor progression and invasion. Evaluating its expression in colorectal cancer and its relation with different clinicopathological parameters can provide valuable information about its role in colorectal cancer progression and behavior.Methods: This retrospective study was conducted on tissue samples of colorectal cancer. The STC2 immunohistochemical expression was detected and evaluated in 60 cases of colorectal cancer tissue samples of formalin-fixed and paraffin-embedded blocks. Then statistical analysis was performed to assess the relationship between its expression level and several clinicopathological parameters in the studied cases.Results: Statistically significant associations were found between the high level of STC2 immunohistochemical expression and histological tumor grade (P

Background & Objective: Colorectal cancer is the third most common cause of cancer death worldwide. Stanniocalcin 2 (STC2) is a glycoprotein hormone over-expressed in many human cancers where it regulates tumor progression and invasion. Evaluating its expression in colorectal cancer and its relation with different clinicopathological parameters can provide valuable information about its role in colorectal cancer progression and behavior. Methods: This retrospective study was conducted on tissue samples of colorectal cancer. The STC2 immunohistochemical expression was detected and evaluated in 60 cases of colorectal cancer tissue samples of formalin-fixed and paraffin-embedded blocks. Then statistical analysis was performed to assess the relationship between its expression level and several clinicopathological parameters in the studied cases. Results: Statistically significant associations were found between the high level of STC2 immunohistochemical expression and histological tumor grade (P<0.001), tumor depth of invasion (T stage) (P=0.004), lymph node metastasis (N stage) (P=0.001), tumor Dukes' stage (P<0.001), the presence of lymphovascular invasion (P<0.001), and perineural invasion (P<0.001). Conclusion: STC2 over-expression in colorectal cancer may be associated with more aggressive tumor behavior including increased tumor invasion, higher histological grade, higher rate of nodal metastasis and increased incidence of lymphovascular and perineural invasions. These data suggest a potential role for STC2 as a predictive biomarker for tumor behavior in colorectal cancer patients. [ABSTRACT FROM AUTHOR]

Epidemiological studies have shown that air pollution and particulate matter (PM) are closely related to the occurrence of cancer. However, the potential prognostic and immunological biomarkers for air pollution related cancers are lacking. In this study, we proved PM2.5 exposure was correlated with lung cancer through transcriptome analysis. Importantly, we identified STC2 as a key gene regulated by PM2.5, whose expression in epithelial cells was significantly increased after PM2.5 treatment and validated by using RT-qPCR and immunofluorescence. Kaplan-Meier OS curves suggested that high STC2 expression positively correlated with a poor prognosis in lung cancer. Furthermore, we discovered that STC2 was associated with multiple cancers and pathways in cancer. Next, Pan-Cancer Expression Landscape of STC2 showed that STC2 exhibited inconsistent expression across 26 types of human cancer, lower in KIRP in cancer versus adjacent normal tissues, and significantly higher in another cancers. Cox regression results suggested that STC2 expression was positively or negatively associated with prognosis in different cancers. Moreover, STC2 expression was associated with clinical phenotypes including age, gender, stage and grade. Mutation features of STC2 were also analyzed, in which the highest alteration frequency of STC2 was presented in KIRC with amplification. Meanwhile, the effects of copy number variation (CNV) on STC2 expression were investigated across various tumor types, suggesting that STC2 expression was significantly correlated with CNV in tumors. Additionally, STC2 was closely related to tumor heterogeneity, tumor stemness and tumor immune microenvironment like immune cell infiltration. In the meantime, we analyzed methylation modifications and immunological correlation of STC2. The results demonstrated that STC2 expression positively correlated with most RNA methylation genes and immunomodulators across tumors. Taken together, the findings revealed that PM2.5-induced STC2 might be a potential prognostic and immunological biomarker for cancers related to air pollution., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Zhu, Liu, Wang, Zhang, Jiang, Liu, Xiong, He and Li.)