BREAKING! Study Finds That Cancer Causing Genes Are Upregulated In SARS-CoV-2 Infected Individuals!
Source: Medical News - SARS-CoV-2 & Cancer Aug 04, 2022 2 years, 4 months, 1 day, 10 hours, 32 minutes ago
SARS-CoV-2 And Cancers: Since the start of the COVID-19 pandemic, numerous scientists have been worried about the post-infection long term health effects of the SARS-CoV-2 virus as it has been known that most viruses can cause long term damages to the host body, some resulting in fatal outcomes. DNA Viruses like Epstein-Barr virus, human papilloma virus, hepatitis B virus, and human herpes virus-8 and RNA viruses like human T lymphotrophic virus type 1 and hepatitis C viruses are already known to be able to cause development of cancers.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1994798/
Thailand
Medical News had been warning about the possibility of the SARS-CoV-2 viruses being oncogenic while many doctors were reporting a sudden rise of what is known as accelerated aggressive cancers over the last 18 months. Many subsequent studies also indicated that SARS-CoV-2 was capable of triggering various cancers. However there seems to be a concerted effort by authorities at the U.S. CDC, U.S.NIH. WHO, ECDC and other relevant agencies to either conceal or down play the carcinogenic effects of the SARS-CoV-2 virus.
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It should also be noted that as a result of SARS-CoV-2 either damaging or dysregulating various immune cells, cancers cells are unchecked in the early stages and are allowed to proliferate even rapidly.
A new bioinformatics study has alarmingly found individuals infected with the SARS-CoV-2 coronavirus have an upregulation of various oncogenic genes especially in the peripheral blood mononuclear cells (PBMCs).
The study team from Tehran University of Medical Sciences observing that the relation between SARS-CoV-2 infection and cancer has been less addressed, aimed to discover any possible links between SARS-CoV-2 infection and cancer development in a bioinformatics study.
For the study, the pertinent datasets were chosen from the GEO database. COVID-19 was searched for differentially expressed genes where |Log2 FC| > 1 and P < 0.05 were deemed statistically significant. The ClusterProfiler package employed gene ontology and pathway enrichment analysis for common genes. Functional interaction of proteins was predicted using STRING online then Cytoscape analysis was carried out to determine the target genes. Finally, gene set enrichment analysis was performed to find any correlation between candidate genes and different types of cancer.
The SARS-CoV-2 And Cancers study findings shockingly showed that numerous cancer-related genes were up-regulated in SARS-CoV-2 infected patients, particularly those genes participating in the cell cycle regulation or engaged in cellular senescence processes.
The study findings suggested that SARS-CoV-2 can be considered a potential risk factor for increasing the probability of developing cancer.
The study findings were published on a peer review platform: Research Square, and are currently being peer reviewed.
https://www.researchsquare.com/article/rs-1894265/v1
Though the SARS-CoV-2 predominantly is a pulmonary disease, but other complications such as heart failure, brain damage and kidneys impairment have been reported. To date, limited studies have described SARS-CoV-2 as a potential risk factor for developing cancer.
Former analysis on transcriptomic databases suggested that SARS-CoV-2 induces the expression of the host transcription factors which also could be identified in NHBE, A549, and Calu-3 lung cancer cell lines. In the course of SARS-CoV-2 invasion host immune checkpoints and cytokine pathways such as programmed death ligand 1 (PDL1), PDL2, interleukin 6 (IL 6), type II interferon, and NF-Kappa B (NF-κB) are activated in order to wipe-out the infection. These pathways also manifested in cancer cell lines similar to host reaction against SARS-CoV-2.
https://www.nature.com/articles/s41598-021-82221-4
A past bioinformatic study analyzed the gene expression pattern of 10 most life-threatening cancers. The TCGA database results demonstrated up-regulation of CREB1, PTEN, SMAD3, and CASP3 genes in pancreatic adenocarcinoma. Based on their conclusion, SARS-CoV-2 potentially could induce the expression of these genes through interaction with angiotensin-converting enzyme 2 (ACE2) on the cell surface of pancreatic cells.
https://pubmed.ncbi.nlm.nih.gov/34155232/
It has also been suggested that SARS-CoV-2 is involved in tumorigenesis mechanisms that control cell proliferation, death, migration as well as immune system responses.
https://www.nature.com/articles/s41598-021-84780-y
Due to the complexity of SARS-CoV-2 pathogenicity, the long-term health consequences demand more investigations. In this context, this new study findings revealed that the up-regulated genes in COVID-19 is similar to cancer processes at least in three different categories including: cell cycle regulation, viral carcinogenesis, and cellular senescence.
It should be noted that the most characteristic feature of cancer development is dysregulation of the cell cycle machinery.
https://pubmed.ncbi.nlm.nih.gov/35271993/
Importantly, the cell cycle regulatory mechanism is tightly associated with the cellular processes of proliferation, differentiation, and apoptosis.
https://pubmed.ncbi.nlm.nih.gov/19561645/
It has been found that any disruption in the cell cycle regulation leads to molecular changes that results in aberrant biological behavior of cancer cells.
https://pubmed.ncbi.nlm.nih.gov/35247630/
This includes resistance to DNA damages, apoptosis and anti-mitotic programs as well as activation of oncogenes or deactivation of tumor suppressor genes that are mediated by cell cycle regulatory mechanisms.
https://pubmed.ncbi.nlm.nih.gov/27801298/
Alarmingly, this new study findings found that 17 cell cycle-related genes were up-regulated in SARS-CoV-2 patients including: CCNB2, ESPL1, TTK, CCNA2, CCNB1, CDC6, CDC20, CDK1, BUB1, CHEK1, BUB1B, CDC45, PLK1, CCNA1, ORC1 AND E2F1. Any dysregulation in the expression of these genes is linked with various cancers, such as breast cancer, digestive tract cancer, bone cancer, endometrial cancer, skin cancer, brain cancer, lung cancer and so on.
The cyclin B2 (CCNB2) is a cell cycle regulator and a member of B-type cyclins superfamily.
https://pubmed.ncbi.nlm.nih.gov/17533373/
CCNB2 deficiency causes the G2/M checkpoint to fail during the cell cycle, resulting in gene mutations and cancer.
https://pubmed.ncbi.nlm.nih.gov/20404349/
The role of CCNB2 in the development of various cancers and metastatic conditions has also been documented. Its overexpression is associated with poor prognosis in hepatocellular carcinoma (HCC) patients.
https://pubmed.ncbi.nlm.nih.gov/31101236/
Targeting CCNB2 via miR-582-3p seems to inhibit the proliferation of acute myeloid leukemia.
https://pubmed.ncbi.nlm.nih.gov/31844417/
An up-regulated expression of CCNB2 was noted in human triple-negative breast cancer (TNBC) cells which ultimately contributed to some pathological features in TNBC patients. In addition, CCNB2 increases the proliferation of TNBC cells In Vitro and causes TNBC tumors in mice.
https://pubmed.ncbi.nlm.nih.gov/34354775/
Viruses are one of the well-known causes of various malignancies in human.
https://pubmed.ncbi.nlm.nih.gov/24468737/
So far, seven human oncoviruses have been associated with malignancies. These include high-risk types of human papilloma virus (HPV), hepatitis B and hepatitis C viruses (HBV and HCV), Epstein-Barr virus (EBV) and Kaposi’s Sarcoma-Associated Herpesvirus (KSHV), Merkel cell polyomavirus (MCPyV), and human T-cell leukemia virus I (HTLV-1).
https://pubmed.ncbi.nlm.nih.gov/17940621/
The detailed pathophysiology of this carcinogenic potential in viruses affecting humans is not fully understood. It seems, oncogenic viruses share similar characteristics that enable them to cause cancer.
https://pubmed.ncbi.nlm.nih.gov/30143749/
In this regard, the study findings showed 12 up-regulated genes with possible relation to viral carcinogenesis in SARS-CoV-2 blood sample, including: H4C8, H2BC7, CDC20, H2BC5, CDK1, H2BC17, H2BC9, CHEK1, EIF2AK2, CCNA1, H2BC8 and CCNA2.
Though for the most part, these genes contribute to viral replication, dysregulation in expression of these genes could disrupt cellular processes such as apoptosis and cell-cycle checkpoints that consequently leads to malignancy.
https://pubmed.ncbi.nlm.nih.gov/24906315/
https://pubmed.ncbi