Curcumin is a polyphenolic compound derived from Curcumin longa L. There are growing bodies of evidence revealing the antitumor effect of curcumin in different tumors; although the molecular mechanism behind this inhibition in glioblastoma multiform (GBM) still remains unclear. Here we investigated the antitumor activity of nano micelles curcumin compared with erlotinib in U‐373 cells in monolayer cell cultures and spheroids models. Furthermore, we characterized affecting cell cycle perturbation, as well as apoptosis induction in GBM cells. The antiproliferative activity of nano micelles curcumin and erlotinib were assessed in monolayer and spheroid models. The influence of the cell cycle and expression levels of nuclear factor κB (NF‐κB) and Wnt/β‐catenin pathway was checked. Nano micelles curcumin suppressed cell growth in U‐373 cells via modulation of Wnt and NF‐κB pathways. Moreover, cells developed an early G2/M cell cycle arrest followed by sub‐G1 apoptosis and apoptotic bodies formation posttreatment with nano micelles curcumin and erlotinib. In the core signaling pathways of GBM, nano micelles curcumin either significantly influences the NF‐κB pathway by decreasing p‐65 expression or significantly inhibits the Wnt/β‐catenin pathway by declining cyclin D1 expression. In conclusion, we have shown that nano micelles curcumin effectively prevent proliferation, and invasion of GBM cells through perturbation of Wnt/β‐catenin and NF‐κB pathways, suggesting further investigations on the therapeutic application of this novel anticancer drug in in vivo models.

According to GLOBOCAN 2012, the worldwide burden of cancer increased and is expected to worsen within the next decades. Therefore, universal combat against cancer will not succeed with treatment solely; effective prevention and early detection are urgently needed to tackle the cancer crisis. Emerging data demonstrate that long non-coding RNAs are involved in numerous biological and pathological processes like development and differentiation and in a variety of human diseases including cancer. Located at 18q21, LINC-ROR (regulator of reprogramming) is a modulator of ESCs maintenance and hypoxia-signaling pathways in hepatocellular cancer cells. The aim of this study was to examine the expression of LINC-ROR in various cell lines and representative samples of human cancers by quantitative real-time RT-PCR to provide a snapshot on how LINC-ROR expression may be deregulated in cancer. More than 30 cell lines and 112 patient specimens from various tissues were assessed for relative expression of LINC-ROR. Our results revealed that the expression of LINC-ROR was lower in all somatic cancer cell lines compared to stem cells or cells with stem cell-like capabilities, like the embryonic carcinoma cell line, NTERA-2. In tissues, expression patterns vary, but some cancerous tissues displayed increased LINC-ROR expression compared to corresponding normal tissues. Thus, we hypothesize that LINC-ROR may have a key function in a subpopulation of cells from the tumor bulk, i.e., the cancer stem cells associated with specific properties including resistance to adverse environmental conditions.

Background Lung cancer is a leading cause of cancer morbidity and mortality worldwide. Several studies have suggested that Human papillomavirus (HPV) infection is an important risk factor in the development of lung cancer. In this study, we aim to address the role of HPV in the development of lung cancer mechanistically by examining the induction of inflammation and epithelial-mesenchymal transition (EMT) by this virus. Methods In this case-control study, tissue samples were collected from 102 cases with lung cancer and 48 controls. We examined the presence of HPV DNA and also the viral genotype in positive samples. We also examined the expression of viral genes (E2, E6 and E7), anti-carcinogenic genes (p53, retinoblastoma (RB)), and inflammatory cytokines in HPV positive cases. Results HPV DNA was detected in 52.9% (54/102) of the case samples and in 25% (12/48) of controls. A significant association was observed between a HPV positive status and lung cancer (OR = 3.37, 95% C.I = 1.58–7.22, P = 0.001). The most prevalent virus genotype in the patients was type 16 (38.8%). The expression of p53 and RB were decreased while and inflammatory cytokines were increased in HPV-positive lung cancer and HPV-positive control tissues compared to HPV-negative lung cancer and HPV-negative control tissues. Also, the expression level of E-cad and PTPN-13 genes were decreased in HPV- positive samples while the expression level of SLUG, TWIST and N-cad was increased in HPV-positive samples compared to negative samples. Conclusion Our study suggests that HPV infection drives the induction of inflammation and EMT which may promote in the development of lung cancer.

Purpose The purpose of this paper is to prioritize lean production (LP) and agile production (AP) factors based on costs of quality (COQ). Design/methodology/approach After literature review, two separated houses of quality (HoQ) have been developed. By the first HoQ, LP and AP factors can be proritized based on prevention and appraisal costs and by the second HoQ, LP and AP factors can be prioritized based on failure costs. The proposed approach has been examined by analyzing data collected from 36 home appliance producers of Isfahan as an industrial province of Iran. Findings The first HoQ indicates that the highest and the lowest priorities are related to over-production (lean factor) and speed (agility factor), respectively. The second HoQ implies that the highest and the lowest priorities are related to responsiveness (agility factor) and inventory (lean factor), respectively. Quadrant analysis also indicates that defectives and over-processing are the two factors that have the highest priorities based on both failure costs and appraisal and prevention costs. As a major finding, LP factors have strong relationship with prevention and appraisal costs; and AP factors have strong relationship with failure costs. Practical implications The proposed approach helps organizations in reducing their costs. By clarifying the relationship of the LP and AP factors and the COQ, managers can determine appropriate strategies with the lowest cost. Originality/value The integrated approach of this study has not been applied and studied in the literature. The subject of the relationship of LP and AP and COQ is relatively new, which integrates the two areas of production management and quality management.

The tumor microenvironment (TME) is a significant contributor to cancer progression containing complex connections between cellular and chemical components and provides a suitable substrate for tumor growth and development. Growing evidence shows targeting tumor cells while ignoring the surrounding TME is not effective enough to overcome the cancer disease. Fibroblasts are essential sentinels of the stroma that due to certain conditions in TME, such as oxidative stress and local hypoxia, become activated, and play the prominent role in the physical support of tumor cells and the enhancement of tumorigenesis. Activated fibroblasts in TME, defined as cancer-associated fibroblasts (CAFs), play a crucial role in regulating the biological behavior of tumors, such as tumor metastasis and drug resistance. CAFs are highly heterogeneous populations that have different origins and, in addition to their role in supporting stromal cells, have multiple immunosuppressive functions via a membrane and secretory patterns. The secretion of different cytokines/chemokines, interactions that mediate the recruitment of regulatory immune cells and the reprogramming of an immunosuppressive function in immature myeloid cells are just a few examples of how CAFs contribute to the immune escape of tumors through various direct and indirect mechanisms on specific immune cell populations. Moreover, CAFs directly abolish the role of cytotoxic lymphocytes. The activation and overexpression of inhibitory immune checkpoints (iICPs) or their ligands in TME compartments are one of the main regulatory mechanisms that inactivate tumor-infiltrating lymphocytes in cancer lesions. CAFs are also essential players in the induction or expression of iICPs and the suppression of immune response in TME. Based on available studies, CAF subsets could modulate immune cell function in TME through iICPs in two ways; direct expression of iICPs by activated CAFs and indirect induction by production soluble and then upregulation of iICPs in TME. With a focus on CAFs’ direct and indirect roles in the induction of iICPs in TME as well as their use in immunotherapy and diagnostics, we present the evolving understanding of the immunosuppressive mechanism of CAFs in TME in this review. Understanding the complete picture of CAFs will help develop new strategies to improve precision cancer therapy.

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At present, effective vaccines have been developed as the most successful approaches for preventing widespread infectious disease. The global efforts are focusing with the aim of eliminating and overcoming the Coronavirus Disease 2019 (COVID-19) and are developing vaccines from the date it was announced as a pandemic disease. In this study, PubMed, Embase, Cochrane Library, Clinicaltrial.gov, WHO reports, Science Direct, Scopus, Google Scholar, and Springer databases were searched for finding the relevant studies about the COVID-19 vaccines. This article provides an overview of multiple vaccines that have been manufactured from December 2020 up to April 2021 and also offers a perspective on their efficacy, safety, advantages, and limitations. Currently, there are several categories of COVID-19 vaccines based on Protein Subunit (PS), Inactivated Virus (IV), Virus Like Particle (VLP), Live Attenuated Virus (LAV), Viral Vector (replicating) (VVr) and Viral Vector (non-replicating) (VVnr) in progress or finalized as indicated by the WHO reporting of April 1, 2020.

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy characterized by early invasiveness and resistance to treatment. Surgery in early stages is the only effective treatment, thus finding new biomarkers for the early detection of PDAC remains a major challenge. The present study aimed to compare the immunoproteome between PDAC patients and healthy controls using serological proteome analysis method. Firstly, cell lysates from two different pancreatic cancer cell lines were separated by two dimensional (2D) gels, and then transferred onto membranes probed with sera from 20 PDAC patients and 10 healthy controls. Proteins differentially reacting with autoantibodies in PDAC patients and control groups and were identified using mass spectrometry. This process led to the identification of 18 pancreatic immunoreactive antigens such as laminin, superoxide dismutase, ATP synthase, Rho GDP-dissociation inhibitor II, septin, glyceraldehyde 3-phosphate-dehydrogenase, phosphoglycerate mutase B, tubulin β8 channel and prohibit in. In the present study, we identified 18 immunoreactive proteins in PDAC. While the identified proteins were critically involved in PDAC pathogenesis, further investigation in a large scale population will determine the applicability of these potential biomarkers for the early diagnosis or treatment of the disease.