Ribonucleotide reductase regulatory subunit M2 (RRM2) is a rate‑limiting enzyme for DNA synthesis and repair. RRM2 has vital roles in controlling the progression of cancer. In the present study, we investigated the RRM2 level in neuroblastoma tissues, analyzed its relationship with clinicopathological characteristics of neuroblastoma patients, and explored the effect of RRM2 on the biological functions of neuroblastoma cells. RRM2 levels in 67 pairs of neuroblastoma and matched adjacent non‑cancerous tissues were detected by qRT‑PCR, and its association with patient clinicopathological features was assessed. Using RRM2 siRNA, the role of RRM2 in cell viability was detected by CCK‑8 assay, and the effects on cell cycle distribution and cell apoptosis were detected by flow cytometry. Hoechst 33342 staining was also performed. For RRM2 protein detection in cells and tissues, western blot analyses were employed. Our results revealed that RRM2 expression was significant higher in neuroblastoma tissues than that noted in adjacent non‑cancerous tissues at both the mRNA and protein levels. The increased RRM2 level was significantly associated with clinical stage. RRM2 levels were suppressed in stage III and IV tumors in the chemotherapy subgroup, compared with levels noted in tumors in the preoperative non‑chemotherapy subgroup. RRM2 siRNA significantly inhibited cell viability in the SH‑5Y5Y cells, induced cell arrest in the G0/G1 phase, and enhanced cell apoptosis. Taken together, overexpression of RRM2 is associated with the genesis and progression of neuroblastoma, and may be a potential chemotherapeutic target.
Background: Increasing attention has been drawn the prognostic value of inflammatory indices for colorectal cancer (CRC). However, the prognostic value of the preoperative C-reactive protein to prealbumin ratio (CPAR) in CRC remains unclear. Methods: A retrospective study was conducted with 794 patients who had CRC and underwent radical surgical resection. The predictive performance of the inflammatory indices was analyzed and compared using the area under the timedependent receiver operating characteristic curve. A competing risk regression model and Cox proportional hazard model were used to analyze the effects of CPAR on disease-free survival (DFS) and overall survival (OS), respectively. Results: Patients with high CPAR (>7.25) had poor survival outcome. The CPAR had the best predictive performance among all inflammatory indices, and was significantly associated with several characteristics of tumor invasion, including histological grade, tumor stage, and tumor size. Multivariate analysis showed that high CPAR was independently associated with poor DFS (subdistribution hazard ratio = 2.28, 95% confidence interval [CI]: 1.74-2.82) and OS (hazard ratio = 1.78, 95% CI: 1.60-1.96). Conclusion:Preoperative CPAR assessment could serve as an effective and reliable tool for prognostic prediction in patients with resectable CRC.colorectal cancer, C-reactive protein to prealbumin ratio, disease-free survival, inflammatory index, overall survival | INTRODUCTIONGlobally, colorectal cancer (CRC) is the third most common malignancy and the second leading cause of cancer death. 1 There have been great improvements in our understanding of its etiology, risk factor, molecular biology, and clinical aspects over the past decades, but it still accounts for nearly 10% of the global cancer burden, with over 1.9 million new diagnoses and 0.9 million deaths in 2020. 2 Radical surgery is the preferred treatment for patients with resectable CRC, but for patients who undergo radical resection, the prognosis is still poor, with 60% of patients surviving for 5 years. 3 Tumor progression, including recurrence and distant metastasis, remains a major concern for patients after surgery.
Research has demonstrated that long non-coding RNAs (lncRNAs) are crucial factors in carcinogenesis. LncRNA, cardiac hypertrophy-related factor (CHRF), has been demonstrated to act as an oncogene in a variety of types of tumor. However, its biological function in lung adenocarcinoma remains to be elucidated. The present study aimed to examine the level of CHRF expression in lung adenocarcinoma tissues and cell lines, and to analyze the association between CHRF and clinicopathological characteristics, as well prognosis of patients with lung adenocarcinoma. Loss-of-function assays were performed to determine the biological function of CHRF. The expression of CHRF was markedly upregulated in lung adenocarcinoma tissues and cell lines. Patients exhibiting upregulated CHRF also demonstrated advanced Tumor-Node-Metastasis stage, lymph node metastasis and larger tumor size compared with those exhibiting downregulated CHRF. Results of Cox proportional hazards regression analysis suggested that highly-expressed CHRF may be regarded as an independent prognostic factor of prognosis. In addition, loss-of-function assays indicated that downregulation of CHRF suppressed cell proliferation, migration and invasion, and induced cell cycle arrest and apoptosis. Western blotting revealed that the phosphoinositide-3-kinase/Akt signaling pathway activity is reduced in lung adenocarcinoma following the knockdown of CHRF. Together, these results indicate that lncRNA, CHRF, may serve a critical role in the development and progression of lung adenocarcinoma, and may act as a novel prognostic biomarker and therapeutic target in lung adenocarcinoma.
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