The prognostic role of survivin in colorectal carcinoma remains controversial. This meta-analysis aimed to explore the association between survivin expression and survival outcomes in patients with colorectal carcinoma. A comprehensive literature search for relevant studies published up to April 2013 was performed using PubMed, MEDLINE and ISI Web of Science. Only articles in which survivin was detected by immunohistochemical staining were included. This meta-analysis was done using STATA and Review Manager. A total of 1784 patients from 14 studies were included in the analysis. Our results showed that survivin overexpression in patients with colorectal carcinoma was significantly associated with poor overall survival (hazard ratio, 1.505; 95% confidence interval, 1.197–1.893; P = 0.000) and disease-free survival (hazard ratio, 2.323; 95% confidence interval, 1.687–3.199; P = 0.000). The results indicated that a significant relationship between survivin expression and overall survival was also exhibited in studies with an Asian country (hazard ratio, 1.684; 95% confidence interval, 1.477–1.921), patient number >100 (hazard ratio, 1.604; 95% confidence interval, 1.371–1.877), the cut-off level 50% (hazard ratio, 1.528; 95% confidence interval, 1.056–2.211) and the hazard ratio estimated (hazard ratio, 1.643; 95% confidence interval, 1.262–2.139). Moreover, upregulation of survivin was associated with stages (III/IV vs. I/II: odds ratio, 1.08; 95% confidence interval, 0.80–1.46), the depth of invasion (T3/T4 vs. T1/T2: odds ratio, 1.79; 95% confidence interval 0.67–4.74), lymph node metastasis (positive vs. negative: odds ratio, 1.49; 95% confidence interval, 0.99–2.26), distant metastasis (positive vs. negative: odds ratio, 2.37; 95% confidence interval, 0.99–5.72) and grade of differentiation (well/moderate vs. poor: odds ratio, 1.02; 95% confidence interval, 0.43–2.41), but without significance. The present meta-analysis indicated that upregulation of survivin was associated with poor prognosis in patients with colorectal carcinoma.

The eukaryotic ribosome is a large ribonucleoprotein complex consisting of four types of ribosomal RNA (rRNA) and approximately 80 ribosomal proteins (RPs), forming the 40S and 60S subunits. In all living cells, its primary function is to produce proteins by converting messenger RNA (mRNA) into polypeptides. In addition to their canonical role in protein synthesis, RPs are crucial in controlling vital cellular processes such as cell cycle progression, cellular proliferation, differentiation, DNA damage repair, genome structure maintenance, and the cellular stress response. Viruses, as obligate intracellular parasites, depend completely on the machinery of the host cell for their replication and survival. During viral infection, RPs have been demonstrated to perform a variety of extra-ribosomal activities, which are especially important in viral disease processes. These functions cover a wide range of activities, ranging from controlling inflammatory responses and antiviral immunity to promoting viral replication and increasing viral pathogenicity. Deciphering the regulatory mechanisms used by RPs in response to viral infections has greatly expanded our understanding of their functions outside of the ribosome. Furthermore, these findings highlight the promising role of RPs as targets for the advancement of antiviral therapies and the development of novel antiviral approaches. This review comprehensively examines the many functions of RPs outside of the ribosome during viral infections and provides a foundation for future research on the host–virus interaction.

Circular RNA (circRNA) exists extensively and plays essential roles in serving as microRNA (miRNA) or protein sponges and protein scaffolding in many organisms. However, the profiles and potential functions of the virus-encoded circRNA, including human cytomegalovirus (HCMV)-encoded circular RNAs, remain unclear. In the present study, HCMV-encoded circRNAs profile in human embryonic lung fibroblasts (HELF) with lytic infection was investigated using RNA deep sequencing and bioinformatics analysis. In total, 629 HCMV-encoded circRNAs were identified with various expression patterns in our results. The full sequences and alternative splicings of circUS12, circUL55, and circUL89 were verified by reverse transcriptase-PCR (RT-PCR) with divergent primers followed and Sanger sequencing. Transcription of circUL89 was validated by Northern blot. The HCMV-encoded circRNA-miRNA network analyses revealed the potential function of HCMV-encoded circRNAs during HCMV infection in HELFs. Collectively, HCMV infection deduced abundant HCMV-associated circRNAs during infection, and the HCMV-encoded circRNAs might play important roles in benefiting HCMV infection.

Human cytomegalovirus (HCMV) is a herpes virus with a long replication cycle. HCMV encoded long non-coding RNA termed RNA2.7 is the dominant transcript with a length of about 2.5kb, accounting for 25% of total viral transcripts. Studies have shown that HCMV RNA2.7 inhibits apoptosis caused by infection. The effect of RNA2.7 on other forms of cell death is still unclear. In this work, we found that RNA2.7 deletion significantly decreased the viability of HCMV-infected cells, while treatment with ferroptosis inhibitor Fer-1 rescued the infection-induced cell death, demonstrating an anti-ferroptosis role of RNA2.7. The results further showed that RNA2.7 inhibited ferroptosis via enhancing Ferritin Heavy Chain 1 (FTH1) and Solute Carrier Family 7 Member 11 (SLC7A11) expression in Erastin treated cells without involving other viral components. Pooled Genome-wide CRISPR screening revealed zinc finger protein 395 (ZNF395) as a new regulator repressing the expression of FTH1 and SLC7A11. HCMV RNA2.7 promoted proteasome-mediated degradation of ZNF395 that resulted in upregulation of FTH1 and SLC7A11 to inhibit ferroptosis, therefore maintain survival in host cells and complete replication of virus.