Colorectal cancer (CRC) is a dangerous form of cancer that affects the gastrointestinal tract. It is a major global health concern, and the aggressive behavior of tumor cells makes it difficult to treat, leading to poor survival rates for patients. One major challenge in treating CRC is the metastasis, or spread, of the cancer, which is a major cause of death. In order to improve the prognosis for patients with CRC, it is necessary to focus on ways to inhibit the cancer's ability to invade and spread. Epithelial-mesenchymal transition (EMT) is a process that is linked to the spread of cancer cells, also known as metastasis. The process transforms epithelial cells into mesenchymal ones, increasing their mobility and ability to invade other tissues. This has been shown to be a key mechanism in the progression of colorectal cancer (CRC), a particularly aggressive form of gastrointestinal cancer. The activation of EMT leads to increases in the spread of CRC cells, and during this process, levels of the protein E-cadherin decrease while levels of N-cadherin and vimentin increase. EMT also contributes to the development of resistance to chemotherapy and radiation therapy in CRC. Non-coding RNAs, such as long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), play a role in regulating EMT in CRC, often through their ability to "sponge" microRNAs. Anti-cancer agents have been shown to suppress EMT and reduce the progression and spread of CRC cells. These findings suggest that targeting EMT or related mechanisms may be a promising approach for treating CRC patients in the clinic. 

Unraveling the function of epithelial-mesenchymal transition (EMT) in colorectal cancer: Metastasis, therapy response, and revisiting molecular pathways.

Following radical surgery, patients may suffer a relapse. It is important to identify such patients so that therapy tactics can be modified appropriately. Existing stratification schemes do not display the probability of recurrence with enough precision since locally advanced prostate cancer (PCa) is classified as high-risk but is not ranked in greater detail. Between 40 and 50% of PCa cases belong to the TMPRSS2-ERG subtype that is a sufficiently homogeneous group for high-precision prognostic marker search to be possible. This study includes two independent cohorts and is based on high throughput sequencing and qPCR data. As a result, we have been able to suggest a perspective-trained model involving a deep neural network based on both qPCR data for mRNA and miRNA and clinicopathological criteria that can be used for recurrence risk forecasts in patients with TMPRSS2-ERG-positive, locally advanced PCa (the model uses ALDH3A2 + ODF2 + QSOX2 + hsa-miR-503-5p + ISUP + pT, with an AUC = 0.944). In addition to the prognostic model’s use of identified differentially expressed genes and miRNAs, miRNA–target pairs were found that correlate with the prognosis and can be presented as an interactome network.

/pdf/aldh3a2-odf2-qsox2-and-microrna-503-5p-expression-to-3o8unm6x.pdf

ALDH3A2, ODF2, QSOX2, and MicroRNA-503-5p Expression to Forecast Recurrence in TMPRSS2-ERG-Positive Prostate Cancer

Background PDRG1 are involved in various physiological regulations of cells, include cell proliferation, growth, apoptosis and cell cycle regulation, but their roles in cancer have not been clearly studied. Methods Firstly, we evaluated the expression and prognostic significance of PDRG1 using a pan-cancer analysis of The Cancer Genome Atlas (TCGA) and Genotypic Tissue Expression (GTEx) databases. Secondly, correlations between PDRG1 and pan-cancer immune cells, m6A methylation, tumor mutation burden (TMB), and microsatellite instability (MSI) were investigated. Finally, we explored the relationship between PDRG1 expression and clinical stage in hepatocellular carcinoma (HCC). Results We found that PDRG1 was significantly overexpressed in bladder urothelial carcinoma (BLCA), breast invasive carcinoma (BRCA), cholangiocarcinoma (CHOL), liver hepatocellular carcinoma (LIHC), and other tumor tissues and was associated with prognosis. In addition, PDRG1 was closely associated with pan-cancer immune cells, m6A methylation, TMB, and MSI expression. The expression of PDRG1 in HCC was correlated with clinical stage, and western blot assay confirmed that PDRG1 was significantly overexpressed in HCC tissues. Conclusions PDRG1 may be an important pan-cancer molecular biomarker for diagnosis and prognosis, and our results may provide a theoretical basis for its future clinical application in cancer diagnosis, treatment, and prognosis, and have been preliminarily validated in HCC.

A pan-cancer analysis of the expression and prognostic significance of PDRG1

Polysialic acid (polySia) is a long homopolymer consisting of α2,8-linked sialic acid with tightly regulated expression in humans. In healthy adults, it occurs on cell surface glycoproteins in neuronal, reproductive, and immune tissues; however, it is aberrantly present in many cancers and its overexpression correlates with significantly increased metastasis and poor prognosis. Prompted by the observation that the MCF-7 breast cancer cell line contains only intracellular polySia, we investigated the secretion of polySia from MCF-7 cells. PolySia was found predominantly on soluble proteins in MCF-7 conditioned media, but also on extracellular vesicles (EVs), secreted from the cells. Since MCF-7 cells do not express known polysialylated proteins, we developed a robust method for purifying polysialylated proteins that uses a metabolic labelling strategy to introduce a bioorthogonal functionality into polySia. Using this method we identified three previously unknown polysialylated proteins, and found that two of these proteins - AGR2 and QSOX2 – were secreted from MCF-7 cells. We confirmed that QSOX2 found in EV-depleted MCF-7 cell conditioned media was polysialylated. Herein we report the secretion of polysialic acid on both soluble and EV-associated proteins from MCF-7 cancer cells and introduce a new method to efficiently identify polysialylated proteins. These findings have exciting implications for understanding the roles of polySia in cancer progression and metastasis and for identifying new cancer biomarkers.

A new strategy for identifying polysialylated proteins reveals they are secreted from cancer cells as soluble proteins and as part of extracellular vesicles

This study focuses on Quiescin Q6 sulfhydryl oxidase 2 (QSOX2), a sulfhydryl oxidase enzyme, in breast cancer, specifically emphasizing triple-negative breast cancer (TNBC) and examining its expression patterns and implications for patient prognosis and disease progression. Using publicly available datasets, we conducted a comprehensive analysis of QSOX2 expression in breast cancer (BC) tumor and non-tumor tissues, assessing its specificity across different molecular subtypes. We further explored correlations between QSOX2 expression and patient outcomes, utilizing datasets like TCGA and METABRIC. In addition, we performed in vitro experiments to evaluate QSOX2 expression in BC cell lines and investigate the effects of QSOX2 knockdown on various TNBC cellular processes, including cell proliferation, apoptosis resistance, migration, and the epithelial-to-mesenchymal transition (EMT). Our results reveal significantly elevated QSOX2 expression in BC tumor tissues, particularly in TNBC, and establish an association between high QSOX2 expression and increased patient mortality, cancer progression, and recurrence across various BC subtypes. Notably, QSOX2 knockdown in TNBC cell lines reduces cell proliferation and suppresses migration. Furthermore, we identify a significant link between QSOX2 and integrin β1 (ITGB1), suggesting that QSOX2 enhances ITGB1 stability, subsequently activating downstream signaling pathways. In conclusion, elevated QSOX2 expression emerges as a key factor associated with adverse patient outcomes in BC, particularly in TNBC, contributing to disease progression through various mechanisms, including the modulation of ITGB1 stability. Our findings underscore the potential of targeting QSOX2 as a therapeutic strategy for improving patient prognoses not only in TNBC but also in other BC subtypes. 

Qsox2 Upregulated in Triple-Negative Breast Cancer Exacerbates Patient Prognosis by Stabilizing Integrin Β1

Background: Quiescin Sulfhydryl Oxidase 2 (QSOX2) is a member of the atypical thiol oxidase family and has been reported in several biological processes, but the expression and role of QSOX2 in colorectal cancer (CRC) remains elusive. Methods: The difference of QSOX2 expression, and it’ s relationship with clinicopathological features and prognosis in CRC was analyzed by bioinformatic analysis and validated by clinical CRC specimen cohort. The functional characterisation of QSOX2 in CRC and was investigated through a series of in vitro experiments while the potential signaling pathways were predicted by Gene Set Enrichment Analysis (GSEA). Results: QSOX2 is significantly upregulated in CRC tissues compared with adjacent non-tumor tissues (adjacent NTTs). The chi-square test indicated that high expression of QSOX2 was associated with Pathological stage (P=0.003) and Lymph node metastasis (P=0.003). Logistic regression analysis indicated that high QSOX2 expression was significantly associated with Pathological stage and Lymph node metastasis. Multivariate analysis suggested that high QSOX2 expression served as an independent significant predictor of poor overall survival (OS) (HR, 1.06; 95%CI, 1.00-1.13; P=0.033). The Kaplan-Meier curves showed that CRC patients with high QSOX2 expression exhibited a poor prognosis. Fisher’s exact test was used to examine the correlation of QSOX2 expression in cancer with clinicopathological characteristics while Kaplan–Meier survival analysis, log-rank test, univariate, and multivariate Cox regression models were used to examine whether QSOX2 expression was correlated with OS and disease-free cumulative survival (DFS) for CRC patients during the clinical validation phase. The data suggested that high QSOX2 expression was significant correlated with advanced clinicopathological parameters. In the meantime, CRC patients with a high level of QSOX2 protein expression trended toward correlation with worse OS and DFS compared with those with decreased QSOX2 expression. In vitro data showed that inhibition of QSOX2 suppresses cell proliferation, migration and invasion in CRC cells. In addition, GSEA showed that multiple signaling pathways were enriched in samples with high-QSOX2 expression phenotype. Conclusion: High QSOX2 expression is strongly associated with aggressive clinicopathological characteristics and poor oncological outcomes. QSOX2 might act as a potential prognostic biomarker and therapeutic target for CRC.

Quiescin Sulfhydryl Oxidase 2 Overexpression Predicts Poor Prognosis and Tumor Progression in Patients With Colorectal Cancer: A Study Based on Data Mining and Clinical Verification.

PDRG1 predicts a poor prognosis and facilitates the proliferation and metastasis of colorectal cancer.

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Quiescin Sulfhydryl Oxidase 2 Overexpression Predicts Poor Prognosis and Tumor Progression in Patients With Colorectal Cancer: A Study Based on Data Mining and Clinical Verification.

PDRG1 predicts a poor prognosis and facilitates the proliferation and metastasis of colorectal cancer.