Background BSG (CD147) is a member of the immunoglobulin superfamily that shows roles for potential prognostics and therapeutics for metastatic cancers and SARS-CoV-2 invasion for COVID-19. The susceptibility of malignant cancers to SARS-CoV-2 as well as the correlations between disease outcome and BSG expression in tumor tissues have not been studied in depth. Methods In this study, we explored the BSG expression profile, survival correlation, DNA methylation, mutation, diagnostics, prognostics, and tumor-infiltrating lymphocytes (TILs) from different types of cancer tissues with corresponding healthy tissues. In vitro studies for cordycepin (CD), N6-(2-hydroxyethyl) adenosine (HEA), N6, N6-dimethyladenosine (m⁶₂A) and 5′-uridylic acid (UMP) on BSG expression were also conducted. Results We revealed that BSG is conserved among different species, and significantly upregulated in seven tumor types, including ACC, ESCA, KICH, LIHC, PAAD, SKCM and THYM, compared with matched normal tissues, highlighting the susceptibility of these cancer patients to SARS-CoV-2 invasion, COVID-19 severity and progression of malignant cancers. High expression in BSG was significantly correlated with a short OS in LGG, LIHC and OV patients, but a long OS in KIRP patients. Methylation statuses in the BSG promoter were significantly higher in BRCA, HNSC, KIRC, KIRP, LUSC, PAAD, and PRAD tumor tissues, but lower in READ. Four CpGs in the BSG genome were identified as potential DNA methylation biomarkers which could be used to predict malignant cancers from normal individuals. Furthermore, a total of 65 mutation types were found, in which SARC showed the highest mutation frequency (7.84%) and THYM the lowest (0.2%). Surprisingly, both for disease-free and progression-free survival in pan-cancers were significantly reduced after BSG mutations. Additionally, a correlation between BSG expression and immune lymphocytes of CD56bright natural killer cell, CD56dim natural killer cell and monocytes, MHC molecules of HLA-A, HLA-B, HLA-C and TAPBP, immunoinhibitor of PVR, PVRL2, and immunostimulators of TNFRSF14, TNFRSF18, TNFRSF25, and TNFSF9, was revealed in most cancer types. Moreover, BSG expression was downregulated by CD, HEA, m⁶₂A or UMP in cancer cell lines, suggesting therapeutic potentials for interfering entry of SARS-CoV-2. Conclusions Altogether, our study highlights the values of targeting BSG for diagnostic, prognostic and therapeutic strategies to fight malignant cancers and COVID-19. Small molecules CD, HEA, m⁶₂A and UMP imply therapeutic potentials in interfering with entry of SARS-CoV-2 and progression of malignant cancers.

Estimating the post mortem interval (PMI) is a crucial and contentious issue in forensic research, particularly in criminal cases. Traditional methods for PMI estimation are limited by constraints and inaccuracies. Circular RNA (circRNA), formed through exon or intron looping to create a complete circular structure without a 5′ end cap and a 3′ poly(A) tail, exhibits exceptional stability, abundance, and tissue-specific characteristics that make it potentially valuable for PMI estimation. However, research on the exploration or application of circRNA in PMI estimation has been limited. This study aims to investigate the correlation between circRNA and PMI. In this study, liver tissue samples were collected from mice at six different time points at 4 °C, 18 °C, 25 °C, and 35 °C, respectively. The reference gene 28S rRNA and the biomarker circRnf169 were successfully screened. Quantitative PCR was employed to examine the correlation between circRnf169 levels and PMI. At 4 °C, the level of circRnf169 decreased with prolonged PMI, whereas at 18 °C, 25 °C, and 35 °C, the circRnf169 RNA was degraded rapidly, indicating that circRnf169 is suitable for PMI estimation at low temperatures or early PMI. These findings suggest the establishment of mathematical model for early PMI based on circRnf169 using liver tissue, which may serve as a reliable marker. Further research is required in order to develop more markers in mice and/or to validate these mathematical models in human samples.

As a cellular protease, transmembrane serine protease 2 (TMPRSS2) plays roles in various physiological and pathological processes, including cancer and viral entry, such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Herein, we conducted expression, mutation, and prognostic analyses for the TMPRSS2 gene in pan-cancers as well as in COVID-19-infected lung tissues. The results indicate that TMPRSS2 expression was highest in prostate cancer. A high expression of TMPRSS2 was significantly associated with a short overall survival in breast invasive carcinoma (BRCA), sarcoma (SARC), and uveal melanoma (UVM), while a low expression of TMPRSS2 was significantly associated with a short overall survival in lung adenocarcinoma (LUAD), demonstrating TMPRSS2 roles in cancer patient susceptibility and severity. Additionally, TMPRSS2 expression in COVID-19-infected lung tissues was significantly reduced compared to healthy lung tissues, indicating that a low TMPRSS2 expression may result in COVID-19 severity and death. Importantly, TMPRSS2 mutation frequency was significantly higher in prostate adenocarcinoma (PRAD), and the mutant TMPRSS2 pan-cancer group was significantly associated with long overall, progression-free, disease-specific, and disease-free survival rates compared to the wild-type (WT) TMPRSS2 pan-cancer group, demonstrating loss of functional roles due to mutation. Cancer cell lines were treated with small molecules, including cordycepin (CD), adenosine (AD), thymoquinone (TQ), and TQFL12, to mediate TMPRSS2 expression. Notably, CD, AD, TQ, and TQFL12 inhibited TMPRSS2 expression in cancer cell lines, including the PC3 prostate cancer cell line, implying a therapeutic role for preventing COVID-19 in cancer patients. Together, these findings are the first to demonstrate that small molecules, such as CD, AD, TQ, and TQFL12, inhibit TMPRSS2 expression, providing novel therapeutic strategies for preventing COVID-19 and cancers.

The Han nationality is an ancient and populous people, and different places in China may have their distinct group relationships. Luzhou area, as a crossroads of several provinces in Southwest China, lacks autosomal short tandem repeat (STR) research and population genetics research. In this study, 21 autosomal STR loci were evaluated in 1959 Han-Chinese individuals from Luzhou area. There was no substantial linkage disequilibrium (LD) among the 21 autosomal STR markers, and all markers were in Hardy–Weinberg equilibrium (HWE). The total discrimination power (TDP) and cumulative probability of exclusion (CPE) of the 21 autosomal STR loci were calculated to be 1–9.8505 × 10⁻¹⁶ and 1–1.9406 × 10⁻⁹, respectively. There were 333 alleles for 21 STRs with allelic frequencies ranging from 0.00026 to 0.51302, and the number of alleles ranged from 7 in locus TPOX to 29 in locus Penta E. According to the results of population comparison and population differentiation, historical influences, geographical distribution, cultural integration, and economic development may have an impact on the Luzhou Han population and other Chinese populations. These 21 STR loci were found to enrich autosomal STR information in forensic databases and provide highly informative polymorphisms for our forensic practice in China, including personal identification and parentage testing.