Analysis of Associated Factors, Construction, and Application of a Predictive Model for Lymph Node Metastasis in Colorectal Cancer.

Background: In colorectal cancer (CRC) , understanding lymph node metastasis (LNM) is critical for effective treatment. Better approaches are required for identifying and assessing the risk contributions of factors influencing lymph node metastasis in colorectal cancer. Objective: This study aims to analyze factors associated with LNM in CRC and develop a risk prediction model. Methods: A retrospective cohort study was conducted and a total of 181 CRC patients admitted between March 2020 and April 2023 were selected as research participants. Among them, 47 patients developed LNM, while the remaining 134 did not. Clinical data, including age, sex, pathological stages, were collected. Logistic regression was employed to identify factors influencing LNM in CRC, forming the basis for constructing a risk model. The diagnostic efficiency of this model was assessed through receiver operating characteristic (ROC) curves. Results: Tumor nodules and histological types showed no correlation with LNM in CRC (P > .05). However, pathological staging, vascular and neural invasion, use of VEGF inhibitors, and preoperative CEA were identified as independent risk factors for LNM in CRC (P < .05). The established model demonstrated a good fit with the observations. ROC curve analysis indicated an area under the curve (AUC) of 0.884 for predicting LNM in CRC, signifying excellent predictive performance. Conclusions: The risk model, formulated on factors associated with LNM in CRC, serves as a efficient tool in assessing the probability of LNM. It provides invaluable insights that can significantly enhance clinical approaches to the diagnosis and treatment of CRC in the future.

Upregulation of the long non-coding RNA SPRY4-IT1 predicts poor prognosis in breast cancer.

BACKGROUND: The upregulation of long non-coding RNA SPRY4 intronic transcript 1 (lncRNA SPRY4-IT1) has been observed in breast cancer (BC). However, there is no previous study of the relationship between SPRY4-IT1 and patient prognosis in BC. This study investigated the prognostic value of SPRY4-IT1 in BC patients. METHODS: The relative expression levels of SPRY4-IT1 were detected by RT-qPCR in 102 paired BC tissues and adjacent noncancerous tissues. The association of SPRY4-IT1 expression with clinicopathological features and prognosis was statistically analyzed. RESULTS: The findings revealed that the SPRY4-IT1 expression was significantly upregulated in clinical BC tissues compared to adjacent normal tissues (P < 0.001). Furthermore, the SPRY4-IT1 level was significantly associated with tumor size (P = 0.009), TNM stage (P = 0.0008) and lymph node metastasis (P = 0.01). Using a Kaplan-Meier analysis, it was shown that patients with high SPRY4-IT1 expression had a significantly poor overall survival (OS) rate (P = 0.0056) and a disease-free survival (DFS) rate (P = 0.0001). Moreover, multivariate Cox analysis revealed that SPRY4-IT1 expression was an independent poor prognostic factor for both OS (P = 0.024) and DFS (P = 0.025) in BC patients. CONCLUSIONS: SPRY4-IT1 expression is an independent prognostic factor for patients with BC and may serve as a potential biomarker to predict prognosis in BC patients.

CircRNA_100290 promotes colorectal cancer progression through miR-516b-induced downregulation of FZD4 expression and Wnt/ß-catenin signaling.

Accumulating evidence indicates that circular RNAs (circRNA) exert crucial functions in the development and advance of cancers. CircRNA_100290 has been reported to promote proliferation in oral cancer. However, whether it participates in colorectal cancer (CRC) remains unclear. Here, our report showed that circRNA_100290 level was significantly increased in CRC tissues and cell lines. Besides, circRNA_100290 expression was positively correlated with tumor metastasis while inversely correlated with prognosis. Silencing circRNA_100290 markedly reduced cell proliferation rate, inhibited migration and invasion abilities, but promoted apoptosis in vitro. Mechanistically, our data revealed circRNA_100290 was a competing endogenous RNA (ceRNA) of FZD4 by sponging miR-516b, leading to activation of Wnt/ß-catenin pathway. Rescue assay indicated that FZD4-induced activation of ß-catenin pathway is indispensable for the function of circRNA_100290 in CRC. In summary, our study for the first time revealed a novel regulatory loop of circRNA_100290/miR-516b/FZD4/Wnt/ß-catenin implicated in CRC progression.

The long non-coding RNA AK023948 enhances tumor progression in hepatocellular carcinoma.

The long non-coding RNAs (lncRNAs) have been demonstrated to play pivotal roles in a broad range of processes including tumor biology. However, the exact contributions of lncRNAs to hepatocellular carcinoma (HCC) remain poorly defined. In current study, we have unraveled a novel function of AK023948 in HCC. We found that AK023948 was substantially upregulated in tumor tissues. Meanwhile, higher AK023948 expression correlated with poor survival. Upregulation of AK023948 expression can promote HepG2 and Hep3B proliferation and invasion in in vitro experiments. Furthermore, AK023948 also decreased tumor growth in vivo. The tumorigenic role of AK023948 was partially ascribed to PI3K/Akt/mTOR signaling and AK023948 knockdown decreased pathway activation and tumor growth. These data collectively suggest an oncogenic role for AK023948 and may provide potential insight into therapeutic intervention.

cir-ITCH plays an inhibitory role in colorectal cancer by regulating the Wnt/ß-catenin pathway.

Noncoding RNAs (ncRNAs) are the dominant product of eukaryotic transcription. These products range from short microRNAs (miRNAs) to long intergenic noncoding RNAs (lincRNAs). Circular RNAs composed of exonic sequences represent an understudied form of ncRNA that was discovered more than 20 years ago. Using a TaqMan-based reverse transcriptase polymerase chain reaction assay, we analyzed the relationship between cir-ITCH expression and colorectal cancer (CRC) in a total of 45 CRCs and paired adjacent non-tumor tissue samples. We found that cir-ITCH expression was typically down-regulated in CRC compared to the peritumoral tissue. This result, as well as several follow-up experiments, showed that cir-ITCH could increase the level of ITCH, which is involved in the inhibition of the Wnt/ß-catenin pathway. Therefore, our results showed that cir-ITCH plays a role in CRC by regulating the Wnt/ß-catenin pathway.