scholarly journals Schlafens: Emerging Proteins in Cancer Cell Biology

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2238
Author(s):  
Sarmad Al-Marsoummi ◽  
Emilie E. Vomhof-DeKrey ◽  
Marc D. Basson
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Cell Biology ◽  
Cancer Biology ◽  
Immune Cell ◽  
Biological Functions ◽  
Cancer Types ◽  
Opposing Effects ◽  
High Degree ◽  
Human And Mouse

Schlafens (SLFN) are a family of genes widely expressed in mammals, including humans and rodents. These intriguing proteins play different roles in regulating cell proliferation, cell differentiation, immune cell growth and maturation, and inhibiting viral replication. The emerging evidence is implicating Schlafens in cancer biology and chemosensitivity. Although Schlafens share common domains and a high degree of homology, different Schlafens act differently. In particular, they show specific and occasionally opposing effects in some cancer types. This review will briefly summarize the history, structure, and non-malignant biological functions of Schlafens. The roles of human and mouse Schlafens in different cancer types will then be outlined. Finally, we will discuss the implication of Schlafens in the anti-tumor effect of interferons and the use of Schlafens as predictors of chemosensitivity.

scholarly journals FAM64A Promotes Osteosarcoma Cell Growth and Metastasis and Is Mediated by miR-493

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Ying Jiang ◽  
Chunlei Zhou ◽  
Qiang Gao ◽  
Zhi-Qi Yin ◽  
Jingwen Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Poor Prognosis ◽  
Migration And Invasion ◽  
Tumor Proliferation ◽  
Osteosarcoma Cell ◽  
Aberrant Expression ◽  
Upstream Gene ◽  
Cancer Types

Aberrant expression of FAM64A was correlated with cell proliferation in various cancer types. We examined the expression of FAM64A and the upstream gene miR-493 in OS. The functions of miR-493 were revealed through extensive experiments. We found an increase of FAM64A gene and protein in OS tissues. Overexpression of FAM64A resulted in promoting tumor proliferation, migration, and invasion. The miR-493 targeted and negatively regulated FAM64A. Our data showed that upregulation of FAM64A in OS correlated with poor prognosis.

scholarly journals The Unfolded Protein Response Is Associated with Cancer Proliferation and Worse Survival in Hepatocellular Carcinoma

Cancers ◽  
2021 ◽  
Vol 13 (17) ◽  
pp. 4443
Author(s):  
Ankit Patel ◽  
Masanori Oshi ◽  
Li Yan ◽  
Ryusei Matsuyama ◽  
Itaru Endo ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Unfolded Protein Response ◽  
Cancer Progression ◽  
Cancer Biology ◽  
Immune Cell ◽  
Histological Grade ◽  
Unfolded Protein ◽  
The Unfolded Protein Response ◽  
Protein Response

Hepatocellular carcinoma is a leading cause of cancer death worldwide. The unfolded protein response (UPR) has been revealed to confer tumorigenic capacity in cancer cells. We hypothesized that a quantifiable score representative of the UPR could be used as a biomarker for cancer progression in HCC. In this study, a total of 655 HCC patients from 4 independent HCC cohorts were studied to examine the relationships between enhancement of the UPR and cancer biology and patient survival in HCC utilizing an UPR score. The UPR correlated with carcinogenic sequence and progression of HCC consistently in two cohorts. Enhanced UPR was associated with the clinical parameters of HCC progression, such as cancer stage and multiple parameters of cell proliferation, including histological grade, mKI67 gene expression, and enrichment of cell proliferation-related gene sets. The UPR was significantly associated with increased mutational load, but not with immune cell infiltration or angiogeneis across independent cohorts. The UPR was consistently associated with worse survival across independent cohorts of HCC. In conclusion, the UPR score may be useful as a biomarker to predict prognosis and to better understand HCC.

scholarly journals miRNA-independent function of long noncoding pri-miRNA loci

2021 ◽  
Vol 118 (13) ◽  
pp. e2017562118
Author(s):  
Daniel He ◽  
David Wu ◽  
Soren Muller ◽  
Lin Wang ◽  
Parna Saha ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Cell Biology ◽  
Cell Types ◽  
Dna Looping ◽  
Gene Promoters ◽  
Functional Studies ◽  
A Genome ◽  
Genome Wide Data ◽  
Cell Propagation

Among the large, diverse set of mammalian long noncoding RNAs (lncRNAs), long noncoding primary microRNAs (lnc-pri-miRNAs) are those that host miRNAs. Whether lnc-pri-miRNA loci have important biological function independent of their cognate miRNAs is poorly understood. From a genome-scale lncRNA screen, lnc-pri-miRNA loci were enriched for function in cell proliferation, and in glioblastoma (i.e., GBM) cells with DGCR8 or DROSHA knockdown, lnc-pri-miRNA screen hits still regulated cell growth. To molecularly dissect the function of a lnc-pri-miRNA locus, we studied LOC646329 (also known as MIR29HG), which hosts the miR-29a/b1 cluster. In GBM cells, LOC646329 knockdown reduced miR-29a/b1 levels, and these cells exhibited decreased growth. However, genetic deletion of the miR-29a/b1 cluster (LOC646329-miR29Δ) did not decrease cell growth, while knockdown of LOC646329-miR29Δ transcripts reduced cell proliferation. The miR-29a/b1–independent activity of LOC646329 corresponded to enhancer-like activation of a neighboring oncogene (MKLN1), regulating cell propagation. The LOC646329 locus interacts with the MKLN1 promoter, and antisense oligonucleotide knockdown of the lncRNA disrupts these interactions and reduces the enhancer-like activity. More broadly, analysis of genome-wide data from multiple human cell types showed that lnc-pri-miRNA loci are significantly enriched for DNA looping interactions with gene promoters as well as genomic and epigenetic characteristics of transcriptional enhancers. Functional studies of additional lnc-pri-miRNA loci demonstrated cognate miRNA-independent enhancer-like activity. Together, these data demonstrate that lnc-pri-miRNA loci can regulate cell biology via both miRNA-dependent and miRNA-independent mechanisms.

scholarly journals Insights Into the Function and Clinical Application of HDAC5 in Cancer Management

2021 ◽  
Vol 11 ◽  
Author(s):  
Jun Yang ◽  
Chaoju Gong ◽  
Qinjian Ke ◽  
Zejun Fang ◽  
Xiaowen Chen ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Proliferation ◽  
Regulatory Mechanisms ◽  
Biological Functions ◽  
Multiple Cancer ◽  
Aberrant Expression ◽  
Cancer Management ◽  
Cancer Types ◽  
Proliferation And Invasion

Histone deacetylase 5 (HDAC5) is a class II HDAC. Aberrant expression of HDAC5 has been observed in multiple cancer types, and its functions in cell proliferation and invasion, the immune response, and maintenance of stemness have been widely studied. HDAC5 is considered as a reliable therapeutic target for anticancer drugs. In light of recent findings regarding the role of epigenetic reprogramming in tumorigenesis, in this review, we provide an overview of the expression, biological functions, regulatory mechanisms, and clinical significance of HDAC5 in cancer.

scholarly journals Pan-Cancer Analysis of DNA Methylation Identifies Genes and Biological Functions Associated with Overall Survival

2021 ◽  
Author(s):  
Romola Grace Cavet ◽  
Peng Yue ◽  
Guy Lawrence Cavet
Keyword(s):  
Dna Methylation ◽  
Overall Survival ◽  
Cancer Biology ◽  
Gene Clusters ◽  
The Cancer Genome Atlas ◽  
Biological Functions ◽  
Cancer Types ◽  
Genomic Regions ◽  
The Relationship ◽  
Pan Cancer

DNA methylation influences gene expression and is altered in many cancers, but the relationship between DNA methylation and cancer outcomes is not yet fully understood. If methylation of specific genes is associated with better or worse outcomes, it could implicate genes in driving cancer and suggest therapeutic strategies. To advance our understanding of DNA methylation in cancer biology, we conducted a pan-cancer analysis of the relationship between methylation and overall survival. Using data on 28 tumor types from The Cancer Genome Atlas (TCGA), we identified genes and genomic regions whose methylation was recurrently associated with survival across multiple cancer types. While global DNA methylation levels are associated with outcome in some cancers, we found that the gene-specific associations were largely independent of these global effects. Genes with recurrent associations across cancer types were enriched for certain biological functions, such as immunity and cell-cell adhesion. While these recurrently associated genes were found throughout the genome, they were enriched in certain genomic regions, which may further implicate certain gene families and gene clusters in affecting survival. By finding common features across cancer types, our results link DNA methylation to patient outcomes, identify biological mechanisms that could explain survival differences, and support the potential value of treatments that modulate the methylation of tumor DNA.

scholarly journals Low expression of miR-29a is associated with aggressive biology and worse survival in gastric cancer

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yoshihisa Tokumaru ◽  
Masanori Oshi ◽  
Michelle R. Huyser ◽  
Li Yan ◽  
Masahiro Fukada ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Biology ◽  
Immune Cell ◽  
Prognostic Biomarker ◽  
Residual Tumor ◽  
Gene Sets ◽  
Aggressive Cancer ◽  
Cancer Types ◽  
Gastric Cancer Patients ◽  
Low Expression

AbstractAdvanced gastric cancer (GC) is one of the most lethal cancer types, thus a better understanding of its biology in patients is urgently needed. MicroRNA (miR)-29a is a known tumor suppressive miR that is related to metastasis, but its clinical relevance in GC remains ambiguous. Here, using a large GC patient cohort we hypothesized that low expression of miR-29a in GC is associated with aggressive cancer biology and worse survival. We demonstrated that low miR-29a GC enriched cell proliferation, apoptosis, metastasis, and angiogenesis related gene sets, as well as the higher expression of related genes. Low miR-29a GC was associated with less anti-cancer immune cell infiltration as well as immune related scoring. Low miR-29a GC demonstrated a worse overall survival (OS) as well as disease specific survival (DSS) compared with high expressing miR-29a GC. Notably, low miR-29a expression was the only factor, other than residual tumor status, to be an independent prognostic biomarker of worse OS and DSS. In conclusion, low miR-29a GC was associated with aggressive cancer biology and worse OS as well as DSS. Additionally, low expression of miR-29a was an independent prognostic biomarker of OS and DSS in gastric cancer patients.

scholarly journals Bacterial cell proliferation: from molecules to cells

2020 ◽  
Author(s):  
Alix Meunier ◽  
François Cornet ◽  
Manuel Campos
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Division ◽  
Dna Replication ◽  
Cell Growth ◽  
Bacterial Cell ◽  
Cell Biology ◽  
Molecular Mechanisms ◽  
Cell Physiology ◽  
Precise Knowledge

ABSTRACT Bacterial cell proliferation is highly efficient, both because bacteria grow fast and multiply with a low failure rate. This efficiency is underpinned by the robustness of the cell cycle and its synchronization with cell growth and cytokinesis. Recent advances in bacterial cell biology brought about by single-cell physiology in microfluidic chambers suggest a series of simple phenomenological models at the cellular scale, coupling cell size and growth with the cell cycle. We contrast the apparent simplicity of these mechanisms based on the addition of a constant size between cell cycle events (e.g. two consecutive initiation of DNA replication or cell division) with the complexity of the underlying regulatory networks. Beyond the paradigm of cell cycle checkpoints, the coordination between the DNA and division cycles and cell growth is largely mediated by a wealth of other mechanisms. We propose our perspective on these mechanisms, through the prism of the known crosstalk between DNA replication and segregation, cell division and cell growth or size. We argue that the precise knowledge of these molecular mechanisms is critical to integrate the diverse layers of controls at different time and space scales into synthetic and verifiable models.

scholarly journals Transcriptional census of epithelial-mesenchymal plasticity in cancer

2021 ◽  
Author(s):  
David P. Cook ◽  
Barbara C. Vanderhyden
Keyword(s):  
Immune Cell ◽  
Tumour Progression ◽  
Expression Patterns ◽  
Therapy Resistance ◽  
Tumour Microenvironment ◽  
Regulatory Mechanisms ◽  
Molecular Features ◽  
Limited Scale ◽  
Cancer Types ◽  
High Degree

ABSTRACTEpithelial-mesenchymal plasticity (EMP) contributes to tumour progression, promoting therapy resistance and immune cell evasion. Definitive molecular features of this plasticity have largely remained elusive due to the limited scale of most studies. Leveraging scRNA-seq data from 160 tumours spanning 8 different cancer types, we identify expression patterns associated with intratumoural EMP. Integrative analysis of these programs confirmed a high degree of diversity among tumours. These diverse programs are associated with combinations of various common regulatory mechanisms initiated from cues within the tumour microenvironment. We highlight that inferring regulatory features can inform effective therapeutics to restrict EMP.

scholarly journals COMPARATIVE EFFECT OF KE AND EW PEPTIDES ON NORMAL AND TUMOR IMMUNE CELLS

2019 ◽  
Vol 19 (1S) ◽  
pp. 174-176
Author(s):  
N S Linkova ◽  
E S Mironova ◽  
O M Ivko ◽  
O A Orlova ◽  
A V Dudkov
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Immune Cells ◽  
Immune Cell ◽  
Human Lymphocytes ◽  
Methylation Status ◽  
Experimental Studies ◽  
Comparative Effect ◽  
Lymphoma Cells ◽  
Normal Human

KE and EW peptides have an immunoprotective and oncostatic effect in experimental studies. However, their comparative effect on normal and cancer immune cells has not been carried out yet. The aim of the work is to study the effect of KE and EW peptides on T-lymphocytes and Berkitt lymphoma cells growth in culture. To plot the cell growth curve, the cells were scattered at a concentration of 20,000 per 2 ml. KE and EW peptides were added to cultures at 100 ng/ml. Counting cells was carried out in the Gorjaev’s chamber. KE and EW peptides increased the number of lymphocytes of human blood as compared with the control during 5 days by 64-219%. KE and EW peptides reduced the number of Burkitt lymphoma cells as compared with the control during 5 days by 37-101%. KE and EW peptides decreased tumor immune cell proliferation and increased normal human lymphocytes grow. We suppose, that these effects can be connected with various ways of peptide regulation of methylation status of DNA.

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