Despite advances in cancer detection and therapy, it has been estimated that the incidence of cancers will increase, while the mortality rate will continue to remain high, a fact explained by the large number of patients diagnosed in advanced stages when therapy is often useless. Therefore, it is necessary to invest knowledge and resources in the development of new non-invasive biomarkers for the early detection of cancer and new therapeutic targets for better health management. In this review, we provided an overview on the collagen family as promising biomarkers and on how they may be exploited as therapeutic targets in cancer. The collagen family tridimensional structure, organization, and functions are very complex, being in a tight relationship with the extracellular matrix, tumor, and immune microenvironment. Moreover, accumulating evidence underlines the role of collagens in promoting tumor growth and creating a permissive tumor microenvironment for metastatic dissemination. Knowledge of the molecular basis of these interactions may help in cancer diagnosis and prognosis, in overcoming chemoresistance, and in providing new targets for cancer therapies.

/pdf/collagen-family-as-promising-biomarkers-and-therapeutic-1vrcjkyu.pdf

Collagen Family as Promising Biomarkers and Therapeutic Targets in Cancer

Abstract Immune checkpoint blockade has recently proven effective in subsets of patients with esophageal adenocarcinoma (EAC) but little is known regarding the EAC immune microenvironment. We determined the single cell transcriptional profile of EAC in 8 patients who were treatment-naive ( n = 4) or had received neoadjuvant chemotherapy ( n = 4). Analysis of 52,387 cells revealed 10 major cell subsets of tumor, immune and stromal cells. Prior to chemotherapy tumors were heavy infiltrated by T regulatory cells and exhausted effector T cells whilst plasmacytoid dendritic cells were markedly expanded. Two dominant cancer-associated fibroblast populations were also observed whilst endothelial populations were suppressed. Pathological remission following chemotherapy associated with broad reversal of immune abnormalities together with fibroblast transition and an increase in endothelial cells whilst a chemoresistant epithelial stem cell population correlated with poor response. These findings reveal features that underlie and limit the response to current immunotherapy and identify a range of novel opportunities for targeted therapy. 

/pdf/the-single-cell-transcriptional-landscape-of-esophageal-1ergqaiq.pdf

The single cell transcriptional landscape of esophageal adenocarcinoma and its modulation by neoadjuvant chemotherapy

miR-145-5p is a microRNA whose role in diverse disorders has been verified. This miRNA is encoded by MIR145 gene on chromosome 5. This miRNA is mainly considered as a tumor suppressor miRNA in diverse types of cancers, including bladder cancer, breast cancer, cervical cancer, cholangiocarcinoma, renal cancer, and gastrointestinal cancers. However, few studies have reported up-regulation of this miRNA in some cancers. Moreover, it has been shown to affect pathogenesis of a number of non-malignant conditions such as aplastic anemia, asthma, cerebral ischemia/reperfusion injury, diabetic nephropathy, rheumatoid arthritis and Sjögren syndrome. In the current review, we summarize the available literature about the role of miR-145-5p in these conditions. 

Function of miRNA-145-5p in the pathogenesis of human disorders.

TGF-β2-induced circ-PRDM5 regulates migration, invasion, and EMT through the miR-92b-3p/COL1A2 pathway in human lens epithelial cells

A novel bioavailable curcumin-galactomannan complex modulates the genes responsible for the development of chronic diseases in mice: A RNA sequence analysis

Background To undertake a bioinformatics analysis to identify abnormally expressed genes [also referred to as differentially expressed genes (DEGs)] and their functions in esophageal carcinoma (ESCA). Methods DEGs (i.e., GSE100942, GSE17351, GSE26886, and GSE77861) were obtained from a gene expression omnibus database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed using online tools from the Database for Annotation, Visualization and Integrated Discovery. A protein-protein interaction network was then constructed based on the Search Tool for the Retrieval of Interacting Genes website. Cytoscape software was used to identify the top 20 DEGs located in the central region of the network. For the overall survival analysis, a Kaplan-Meier analysis was conducted of the Gene Expression Profiling Interactive Analysis website, and collagen (COL) 1A2 was selected to detect the molecular mechanism of COL1A2-small interfering ribonucleic acid (siRNA) in the following ESCA cell lines: Eca109 and TE-1. Next, the expression of COL1A2-messanger ribonucleic acid was determined using real-time quantitative polymerase chain reaction. The expression of COL1A2 was also verified by Western blot. Cell proliferation was measured by colony-forming and MTT assays, and migration and invasion by the transwell assay. Results Based on the GEO database and screening out the hub gene, we identified that COL1A2 was abnormally expressed in ESCA. With a series of in vitro experiments, the expression of COL1A2 was defined as higher in Eca109 and TE-1. Conclusions COL1A2 was highly expressed in ESCA tissue samples. Additionally, the proliferation and metastasis of Eca109 and TE-1 cell lines were significantly attenuated by siRNA-COL1A2-mediated small interference. Notably, the expression level of COL1A2 was obviously related to the Akt and epithelial-mesenchymal transition (EMT) pathways.

/pdf/high-expression-of-collagen-1a2-promotes-the-proliferation-1snn25in6v.pdf

High expression of collagen 1A2 promotes the proliferation and metastasis of esophageal cancer cells

Objective To screen lung adenocarcinoma (LUAC)-specific cell-cycle-related genes (CCRGs) and develop a prognostic signature for patients with LUAC. Methods The GSE68465, GSE42127, and GSE30219 data sets were downloaded from the GEO database. Single-sample gene set enrichment analysis was used to calculate the cell cycle enrichment of each sample in GSE68465 to identify CCRGs in LUAC. The differential CCRGs compared with LUAC data from The Cancer Genome Atlas were determined. The genetic data from GSE68465 were divided into an internal training group and a test group at a ratio of 1:1, and GSE42127 and GSE30219 were defined as external test groups. In addition, we combined LASSO (least absolute shrinkage and selection operator) and Cox regression analysis with the clinical information of the internal training group to construct a CCRG risk scoring model. Samples were divided into high- and low-risk groups according to the resulting risk values, and internal and external test sets were used to prove the validity of the signature. A nomogram evaluation model was used to predict prognosis. The CPTAC and HPA databases were chosen to verify the protein expression of CCRGs. Results We identified 10 LUAC-specific CCRGs (PKMYT1, ETF1, ECT2, BUB1B, RECQL4, TFRC, COCH, TUBB2B, PITX1, and CDC6) and constructed a model using the internal training group. Based on this model, LUAC patients were divided into high- and low-risk groups for further validation. Time-dependent receiver operating characteristic and Cox regression analyses suggested that the signature could precisely predict the prognosis of LUAC patients. Results obtained with CPTAC, HPA, and IHC supported significant dysregulation of these CCRGs in LUAC tissues. Conclusion This prognostic prediction signature based on CCRGs could help to evaluate the prognosis of LUAC patients. The 10 LUAC-specific CCRGs could be used as prognostic markers of LUAC.

/pdf/prognostic-signature-for-lung-adenocarcinoma-patients-based-2ydio532px.pdf

Prognostic Signature for Lung Adenocarcinoma Patients Based on Cell-Cycle-Related Genes.

Mammalian mitochondrial ribosomal proteins are a group of protein factors encoded by nuclear genes, responsible for the synthesis of proteins in mitochondria. As a member of mitochondrial ribosomal proteins, MRPL42 (mitochondrial ribosomal protein L42) belongs to 28S and 39S subunits. The current literature showed that its role in lung adenocarcinoma (LUAD) was not clear. We found that MRPL42 was highly expressed in early-stage LUAD tissues and cell lines, and remarkably related to the prognosis of patients. Knockdown of MRPL42 could reduce the proliferation and colonization, promote cell cycle arrest in G1/S phase, and weaken the migration and invasion ability of LUAD cells in vitro. Moreover, depletion of MRPL42 also inhibited tumor growth in vivo. Bioinformatics analysis found that YY1 may bind to the promoter region upstream of the MRPL42 gene to promote the transcription of MRPL42, which was verified by the ChIP and Dual luciferase reporter assay. QRT-PCR confirmed that knocking down YY1 could attenuate the expression of MRPL42. In summary, MRPL42 acts as an oncogene in LUAD, and its expression level is regulated by YY1.

/pdf/mrpl42-is-activated-by-yy1-to-promote-lung-adenocarcinoma-kfap317d94.pdf

MRPL42 is activated by YY1 to promote lung adenocarcinoma progression

Background In recent years, there have been increasing reports that dysregulated circular RNAs (circRNAs) play a key role in the carcinogenesis of lung adenocarcinoma (LUAC). However, the role of circRNAs in early-stage LUAC is poorly understood. Methods The Gene Expression Omnibus (GEO) database and qRT-PCR were used to verify the abnormal expression of circRNAs, miRNAs and genes in early-stage LUAC tissues. shRNA and miRNA inhibitor are designed and synthesized to knock down circ_104640 and microRNA (miR)-145-5p expression. CCK-8 assay, colony formation assay and flow cytometry were used to study the effect of circ_104640 on cell proliferation and apoptosis. Bioinformatics analysis, dual luciferase reporter assays and argonaute 2 (Ago2) RNA immunoprecipitation (RIP) assays were chosen to find out the potential target of circ_104640. Results Based on the GEO database and tissue sample from our institution, we identified that the circRNA circ_104640, the miR-145-5p, and CCL20 (C-C motif chemokine ligand 20) were abnormally expressed in the tissues of early-stage LUAC. In vitro experiments showed that circ_104640 could exist stably in the cytoplasm, and a short pin RNA that targeted circ_104640 (sh-circ) inhibited cell growth and promoted apoptosis of LUAC cells. Dual luciferase reporter assays and Ago2 (RIP) assays confirmed the Ago2-dependent interaction of circ_104640 and miR-145-5p. In terms of mechanisms, we found that circ_104640 increased the expression of CCL20 by sponging miR-145-5p. Conclusions Our research demonstrated that circ_104640 could accelerate the proliferation of LUAC cells, while inhibiting LUAC cell apoptosis. circ_104640 may be a potential novel biomarker and therapeutic target for early-stage LUAC.

/pdf/the-roles-and-mechanisms-of-the-circular-rna-circ-104640-in-3p798nz0wh.pdf

The roles and mechanisms of the circular RNA circ_104640 in early-stage lung adenocarcinoma: a potential diagnostic and therapeutic target.

Background This study aimed to investigate the relationship between RNA polymerase II subunit 5 (RPB5)-mediating protein (RMP) and clinicopathological characteristics of non-small cell lung cancer (NSCLC) patients by measuring the expression level of RMP in human NSCLC tissues and cell lines. At the same time, we studied the impact of RMP on the biological function of cancer, providing strong support for gene targeted therapy of NSCLC. Methods Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot were used to determine the expression levels of messenger (m)RNA and protein in NSCLC cell lines and tissues. Cell counting kit 8 (CCK8) assay and flow cytometry were selected to detect cell proliferation, cycle and apoptosis. The wound healing assay was chosen to detect the migration and invasion ability of cells. The xenograft model was performed to study the function of RMP in vivo. Immunohistochemical (IHC) staining showed the levels of RMP, Bcl-2, Bax and caspase-3. Results First, mRNA and protein levels of RMP were relatively overexpressed in NSCLC cells. Compared with the corresponding normal tissues, the mRNA and protein levels of RMP were significantly higher in human NSCLC tissues. Concurrently, we found that the expression of RMP was related to the status of lymph nodes (LNs) in cancer tissues and T stage. Then, RMP overexpression promoted the proliferation of A549. At the same time, RMP provided A549 cells the ability to resist chemotherapy and radiotherapy; when A549 cells were treated with gefitinib and radiation, RMP reduced apoptosis. We also found that RMP can protect A549 from G2 block caused by radiation. Over-irradiated RMP-overexpressed A549 cells had lower Bcl2-associated X protein (Bax) levels and higher B-cell lymphoma 2 (Bcl-2) levels. The migration and invasion ability of A549 cells was increased by RMP. Finally, RMP can promote tumor growth by increasing Bcl-2 levels and decreasing Bax and caspase-3 levels in the xenograft model. Conclusions There is potential for RMP to develop into a diagnostic and therapeutic target for NSCLC.

/pdf/rpb5-mediating-protein-promotes-the-progression-of-non-small-5fapzivzgj.pdf

RPB5-mediating protein promotes the progression of non-small cell lung cancer by regulating the proliferation and invasion.

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