Figure - available from: Bioengineered
This content is subject to copyright. Terms and conditions apply.
DCN knockdown improved the negative effect of PGM5-AS1 overexpression on CC cells. (a) EDU assay identified the change of cell proliferation in transfected CC cells. (b) Wound healing assay measured the change of migration rate in transfected CC cells. (c) Transwell assay verified the change of the number of invaded cells in transfected CC cells. **P < 0.001 vs. pcDNA3.1. #P < 0.05, ##P < 0.001 vs. pcDNA-PGM5-AS1.
Source publication
Long non-coding RNAs (lncRNAs) have been widely studied and play crucial roles in cervical cancer (CC) progression. Here, we investigated the function and mechanism of lncRNA PGM5-AS1 action in CC cells. Using real-time quantitative polymerase chain reaction or western blotting, PGM5-AS1 and decorin (DCN) were downregulated in CC tissues and cells,...
Similar publications
Objective
This study analyzed the levels of peripheral blood tumor necrosis factor-α (TNF-α), Decorin (DCN) and Mitogen-activated protein kinase 1 (MAPK1) mRNA in neutrophils of patients with preeclampsia and their correlations, in order to provide more thoughts on the diagnosis and treatment of clinical patients.
Methods
81 patients with preeclam...
Heart failure (HF) remains a global public health burden and often results following myocardial infarction (MI). Following injury, cardiac fibrosis forms in the myocardium which greatly hinders cellular function, survival, and recruitment, thus severely limits tissue regeneration. Here, we leverage biophysical microstructural cues made of hyaluroni...
Evidence for the tumour‐supporting capacities of the tumour stroma has accumulated rapidly in colorectal cancer (CRC). Tumour stroma is composed of heterogeneous cells and components including cancer‐associated fibroblasts (CAFs), small vessels, immune cells, and extracellular matrix proteins. The present study examined the characteristics of CAFs...
Adipose-derived stem cells (ADSCs) are employed as a promising alternative in treating cartilage injury. Regulating the inflammatory "fingerprint" of ADSCs to improve their anti-inflammatory properties could enhance therapy efficiency. Herein, a novel injectable decorin/gellan gum hydrogel combined with ADSCs encapsulation for arthritis cartilage t...
Cervical cancer (CC) is considered to be the most prevalent female malignancies across the globe and a prime cause of mortality among women. RNA-binding motif protein 15 (RBM15) has been elucidated to participate in tumorigenesis in various cancers by regulating RNA N6-methyladenosine (m6A) methylation. However, its significance and detailed molecu...
Citations
... Our study, on the other hand, focused on decorin (DCN) as a downstream target of RBM15, which belongs to the extracellular matrix small leucine-rich proteoglycan class of proteins known to be widely expressed in most tissues (Diehl et al. 2021). In our previous study, we explored the mechanism of DCN in CC by ceRNA mechanism (Wang et al. 2022). ...
... Our previous study showed that DCN was downregulated in CC, but the m6A modification of DCN did not confirm (Wang et al. 2022). Here, we continued to explore whether RBM15 could mediate the m6A modification of DCN. ...
... Its anti-tumor effects have been documented in various malignant tumors, including breast (Reed et al. 2005), colon (Santra et al. 1995), ovarian (Nash et al. 1999), and pancreatic (Koninger et al. 2004) cancers. In our previous study, we discovered the upregulation of DCN in CC, and its expression could be regulated by miR-4284 (Wang et al. 2022). In this study, we deeply investigated the m6A modification of DCN in CC. ...
Cervical cancer (CC) is considered to be the most prevalent female malignancies across the globe and a prime cause of mortality among women. RNA-binding motif protein 15 (RBM15) has been elucidated to participate in tumorigenesis in various cancers by regulating RNA N6-methyladenosine (m6A) methylation. However, its significance and detailed molecular mechanisms remain uncertain in CC. Using CGA database and qRT-PCR, the RBM15 expression was found to be elevated in CC tissues. After performing EdU, wound healing, Transwell migration, and xenograft tumor assays, RBM15 knockdown inhibited the malignant properties of CC cells along with the tumor development of CC cells in vivo. Moreover, qRT-PCR, MeRIP, and western blotting experiments were also confirmed that decorin (DCN) downregulated in CC was a direct substrate of RBM15 m6A methylation, and RBM15 knockdown could enhance DCN expression in CC cells. The anti-tumor effects of RBM15 knockdown could be abolished by DCN silencing. Overall, RBM15 knockdown lowered the tumorigenesis of CC both in vitro and in vivo, and it does so via mediating m6A modification of DCN mRNA in CC cells.
Cervical cancer (CC), the fourth most prevalent type of cancer among women worldwide, is associated with high rates of morbidity and mortality. Due to the long period of latency in CC, most patients are already in the middle to late stages when initially diagnosed, which greatly reduces the clinical cure rate and quality of survival, thus resulting in poor outcomes. In recent years, with continuous exploration in the fields of bioinformatics and molecules, it has been found that ncRNAs, including miRNAs and lncRNAs, without the ability to translate proteins are capable of activating or inhibiting certain signaling pathways by targeting and modulating the level of expression of proteins involved in these signaling pathways. ncRNAs play important roles in assisting with diagnosis, drug administration, and prediction of prognosis during CC progression. As an entry point, the mechanisms of interaction between miRNAs, lncRNAs, and signaling pathways have long been a focus in basic research relating to CC, and numerous experimental studies have confirmed the close relationship of miRNAs, lncRNAs, and signaling pathways with CC development. Against this background, we summarize the latest advances in the involvement of lncRNA- and miRNA-related signaling pathways in the development of CC to provide guidance for CC treatment.
Immunogenic cell death (ICD) in cancer represents a functionally unique therapeutic response that can induce tumor-targeting immune responses. ICD is characterized by the exposure and release of numerous damage-associated molecular patterns (DAMPs), which confer adjuvanticity to dying cancer cells. The spatiotemporally defined emission of DAMPs during ICD has been well described, whereas the epigenetic mechanisms that regulate ICD hallmarks have not yet been deeply elucidated. Here, we aimed to examine the involvement of miRNAs and their putative targets using well-established in vitro models of ICD. To this end, B cell lymphoma (Mino) and breast cancer (MDA-MB-231) cell lines were exposed to two different ICD inducers, the combination of retinoic acid (RA) and interferon-alpha (IFN-α) and doxorubicin, and to non ICD inducers such as gamma irradiation. Then, miRNA and mRNA profiles were studied by next generation sequencing. Co-expression analysis identified 16 miRNAs differentially modulated in cells undergoing ICD. Integrated miRNA-mRNA functional analysis revealed candidate miRNAs, mRNAs, and modulated pathways associated with Immune System Process (GO Term). Specifically, ICD induced a distinctive transcriptional signature hallmarked by regulation of antigen presentation, a crucial step for proper activation of immune system antitumor response. Interestingly, the major histocompatibility complex class I (MHC-I) pathway was upregulated whereas class II (MHC-II) was downregulated. Analysis of MHC-II associated transcripts and HLA-DR surface expression confirmed inhibition of this pathway by ICD on lymphoma cells. miR-4284 and miR-212-3p were the strongest miRNAs upregulated by ICD associated with this event and miR-212-3p overexpression was able to downregulate surface expression of HLA-DR. It is well known that MHC-II expression on tumor cells facilitates the recruitment of CD4+ T cells. However, the interaction between tumor MHC-II and inhibitory coreceptors on tumor-associated lymphocytes could provide an immunosuppressive signal that directly represses effector cytotoxic activity. In this context, MHC-II downregulation by ICD could enhance antitumor immunity. Overall, we found that the miRNA profile was significantly altered during ICD. Several miRNAs are predicted to be involved in the regulation of MHC-I and II pathways, whose implication in ICD is demonstrated herein for the first time, which could eventually modulate tumor recognition and attack by the immune system.
