The regulatory loop between long noncoding RNAs (lncRNAs) and microRNAs has a dynamic role in transcriptional and translational regulation, and is involved in cancer. However, the regulatory ...circuitry between lncRNAs and microRNAs in tumorigenesis remains elusive. Here we demonstrate that a nuclear lncRNA LINC00336 is upregulated in lung cancer and functions as an oncogene by acting as a competing endogenous RNA (ceRNAs). LINC00336 bound RNA-binding protein ELAVL1 (ELAV-like RNA-binding protein 1) using nucleotides 1901-2107 of LINC00336 and the RRM interaction domain and key amino acids (aa) of ELAVL1 (aa 101-213), inhibiting ferroptosis. Moreover, ELAVL1 increased LINC00336 expression by stabilizing its posttranscriptional level, whereas LSH (lymphoid-specific helicase) increased ELAVL1 expression through the p53 signaling pathway, further supporting the hypothesis that LSH promotes LINC00336 expression. Interestingly, LINC00336 served as an endogenous sponge of microRNA 6852 (MIR6852) to regulate the expression of cystathionine-β-synthase (CBS), a surrogate marker of ferroptosis. Finally, we found that MIR6852 inhibited cell growth by promoting ferroptosis. These data show that the network of lncRNA and ceRNA has an important role in tumorigenesis and ferroptosis.
Epstein-Barr virus is an important cancer causing virus. Nasopharyngeal carcinoma is an infection-related cancer strongly driven by Epstein-Barr virus. In this cancer model, we identified the major ...host targets of latent membrane protein 1 which is a driving oncogene encoded by Epstein-Barr virus in latency infection. latent membrane protein 1 activates several oncogenic signaling axes causing multiple malignant phenotypes and therapeutic resistance. Also, Epstein-Barr virus up-regulates DNA methyltransferase 1 and mediates onco-epigenetic effects in the carcinogenesis. The collaborating pathways activated by latent membrane protein 1 constructs an oncogenic signaling network, which makes latent membrane protein 1 an important potential target for effective treatment or preventive intervention. In Epstein-Barr virus lytic phase, the plasma level of Epstein-Barr virus DNA is considered as a distinguishing marker for nasopharyngeal carcinoma in subjects from healthy high-risk populations and is also a novel prognostic marker in Epstein-Barr virus-positive nasopharyngeal carcinoma. Now the early detection and screening of the lytic proteins and Epstein-Barr virus DNA have been applied to clinical and high-risk population. The knowledge generated regarding Epstein-Barr virus can be used in Epstein-Barr virus based precision cancer prevention and therapy in the near future.
Long noncoding RNAs (lncRNA) have been associated with various types of cancer; however, the precise role of many lncRNAs in tumorigenesis remains elusive. Here we demonstrate that the cytosolic ...lncRNA P53RRA is downregulated in cancers and functions as a tumor suppressor by inhibiting cancer progression. Chromatin remodeling proteins LSH and Cfp1 silenced or increased P53RRA expression, respectively. P53RRA bound Ras GTPase-activating protein-binding protein 1 (G3BP1) using nucleotides 1 and 871 of P53RRA and the RRM interaction domain of G3BP1 (aa 177-466). The cytosolic P53RRA-G3BP1 interaction displaced p53 from a G3BP1 complex, resulting in greater p53 retention in the nucleus, which led to cell-cycle arrest, apoptosis, and ferroptosis. P53RRA promoted ferroptosis and apoptosis by affecting transcription of several metabolic genes. Low P53RRA expression significantly correlated with poor survival in patients with breast and lung cancers harboring wild-type p53. These data show that lncRNAs can directly interact with the functional domain of signaling proteins in the cytoplasm, thus regulating p53 modulators to suppress cancer progression.
A cytosolic lncRNA functions as a tumor suppressor by activating the p53 pathway.
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Cancer cells frequently display fundamentally altered cellular metabolism, which provides the biochemical foundation and directly contributes to tumorigenicity and malignancy. Rewiring of metabolic ...programmes, such as aerobic glycolysis and increased glutamine metabolism, are crucial for cancer cells to shed from a primary tumor, overcome the nutrient and energy deficit, and eventually survive and form metastases. However, the role of lipid metabolism that confers the aggressive properties of malignant cancers remains obscure. The present review is focused on key enzymes in lipid metabolism associated with metastatic disease pathogenesis. We also address the function of an important membrane structure-lipid raft in mediating tumor aggressive progression. We enumerate and integrate these recent findings into our current understanding of lipid metabolic reprogramming in cancer metastasis accompanied by new and exciting therapeutic implications.
Mitochondria are the major cellular energy‐producing organelles and intracellular source of reactive oxygen species. These organelles are responsible for driving cell life and death through ...mitochondrial network structure homeostasis, which is determined by a balance of fission and fusion. Recent advances revealed that a number of components of the fission and fusion machinery, including dynamin‐related protein 1 (Drp1), mitofusin1/2 (Mfn1/2) and Optic atrophy 1 (OPA1), that have been implicated in mitochondrial shape changes are indispensible for autophagy, apoptosis and necroptosis. Drp1 is the main regulator of mitochondrial fission and has become a key point of contention. The controversy focuses on whether Drp1 is directly involved in the regulation of cell death and, if involved, whether is it a stimulator or a negative regulator of cell death. Here, we examine the relevance of the homeostasis of the mitochondrial network structure in 3 different types of cell death, including autophagy, apoptosis and necroptosis. Furthermore, a variety of cancers often exhibit a fragmented mitochondrial phenotype. Thus, the fragmented ratio can reflect tumor progression that predicts prognosis and therapeutic response. In addition, we investigate whether the targeting of the mitochondrial fission protein Drp1 could be a novel therapeutic approach.
Here, we examine the relevance of the homeostasis of the mitochondrial network structure in 3 different types of cell death, including autophagy, apoptosis and necroptosis. Furthermore, a variety of cancers often exhibit a fragmented mitochondrial phenotype. Targeting the mitochondrial fission protein Drp1or other shaping proteins is becoming a topic of interest. Further studies are needed to understand the differential effects of oncogenic signaling pathways on mitochondrial dynamics and to identify additional new signaling axes that regulate mitochondrial network structure homeostasis.
Aim
To explore whether plasma microRNA‐16‐5p, ‐17‐5p and ‐20a‐5p can be used as diagnostic biomarkers in gestational diabetes mellitus (GDM) and to investigate the relationship between those ...microRNAs and the risk factors of GDM (body mass index BMI, insulin resistance IR and tumor necrosis factor‐α (TNF‐α)).
Methods
A total of 85 pregnant women with GDM and 72 pregnant women without GDM were enrolled in this study. The plasma concentration of microRNAs (microRNA‐16‐5p, ‐17‐5p, ‐19a‐3p, ‐19b‐3p, ‐20a‐5p) was measured using quantitative reverse transcription–polymerase chain reaction (qRT‐PCR). Spearman's correlation analysis was used to evaluate the correlation between those microRNAs and the risk factors of GDM, and receiver operating characteristic curve analysis was used to evaluate diagnostic sensitivity and specificity.
Results
Compared with non‐GDM women, the relative and absolute expression of plasma microRNA‐16‐5p, ‐17‐5p, ‐20a‐5p from GDM women were significantly upregulated, when those women were diagnosed as GDM. During pregnancy, the expression of those microRNAs from GDM women also were significantly upregulated. The expression of those microRNAs was also positively correlated with IR, a risk factor of GDM. Plasma microRNA‐16‐5p, ‐17‐5p, ‐20a‐5p reflected an obvious separation between GDM women and non‐GDM women, with areas under the curve of 0.92 (95%CI: 0.871–0.984), 0.88 (95%CI: 0.798–0.962), and 0.74 (95%CI: 0.618–0.870), respectively, cut‐offs >2554, 1820, 3886 copies/μL, respectively; sensitivity 41.6%, 21.4% and 17.8%, respectively; and specificity 95.8%, 95.4% and 95.4%, respectively.
Conclusion
Plasma microRNA‐16‐5p, ‐17‐5p and ‐20a‐5p are potential diagnostic biomarkers in GDM.
Macrophages are widely distributed innate immune cells that play indispensable roles in the innate and adaptive immune response to pathogens and in-tissue homeostasis. Macrophages can be activated by ...a variety of stimuli and polarized to functionally different phenotypes. Two distinct subsets of macrophages have been proposed, including classically activated (M1) and alternatively activated (M2) macrophages. M1 macrophages express a series of proinflammatory cytokines, chemokines, and effector molecules, such as IL-12, IL-23, TNF-α, iNOS and MHCI/II. In contrast, M2 macrophages express a wide array of anti-inflammatory molecules, such as IL-10, TGF-β, and arginase1. In most tumors, the infiltrated macrophages are considered to be of the M2 phenotype, which provides an immunosuppressive microenvironment for tumor growth. Furthermore, tumor-associated macrophages secrete many cytokines, chemokines, and proteases, which promote tumor angiogenesis, growth, metastasis, and immunosuppression. Recently, it was also found that tumor-associated macrophages interact with cancer stem cells. This interaction leads to tumorigenesis, metastasis, and drug resistance. So mediating macrophage to resist tumors is considered to be potential therapy.
To solve the problem of high time consumption and energy loss of edge computing perceptual task offloading in the mobile IoT (Internet of things), it is necessary to increase the particle population ...diversity and the performance of escaping the local optimum solution in the intelligent optimization algorithm. For the offloading scenario of multi edge center servers and smart devices of multi IoT users, the NQPSOOM method (A new method of user perceptual task offloading in the IoT based on optimizing strategy of quantum behavior particle population) was proposed. The adaptability variance of the quantum behavior particle population was designed to measure the convergence of the particle population. The logistic chaos perturbation strategy was used to improve the performance of the intelligent optimization algorithm of escaping the local optimum solution. The exchange and mutation operations of fast elite non-dominated sorting genetic algorithm based on crowding coefficient were designed to select the particle population with a high diversity of quantum behavior particle population. Compared with the other five perceptual task computing offloading methods in recent three years, considering the convergence of the perceptual offloading model, the impact of the number of smart devices of IoT users, the number of edge center servers and the perceptual task data size on the optimal offloading method, the NQPSOOM method improves the performance of the perceptual task offloading model, including reducing the adaptability of the intelligent optimization algorithm by 4.89% on average, that is, facilitating the convergence speed of the intelligent optimization algorithm by 4.89%, and lowering the time consumption of the algorithm by 4.08% and energy loss by 3.91% on average.
•New Offloading Method of IoT User Perceptual Task Based on QBPPO was proposed.•The adaptability variance of the quantum behavior particle population was designed.•The logistic chaos perturbation strategy was designed.•Improving the convergence speed of the intelligent optimization algorithm.•Decreasing the time consumption and energy loss of the algorithm.
Silver-based coordination polymers were used to conduct efficiently selective uptake of organic dyes with NH2 &SO3−. The controlled slow-release of Ag+ ions from silver-based CPs leads to excellent ...antibacterial activities towards bacteria.
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Two silver-based coordination polymers, Ag2(bpy)2(cbda) (BUC-51) and Ag3(bpy)3(cpda)·(NO3)·9H2O (BUC-52), have been successfully prepared by slow evaporation at room temperature. These coordination polymers exhibited good adsorptive performances toward series organic dyes with sulfonic groups, which could be ascribed to the AgcdotsO interaction between the silver(I) atoms in CPs and the oxygen atoms from sulfonic groups attached to organic dyes. Both BUC-51 and BUC-52 favoured slow release of Ag+ ions resulting into outstanding long-term antibacterial abilities toward Gram-negative bacteria, Escherichia coli (E. coli), which was tested by a minimal inhibition concentration (MIC) benchmark and an inhibition zone testing method. Both scanning electron microscope (SEM) and transmission electron microscope (TEM) images demonstrated that these two Ag-based coordination polymers could destroy the bacterial membrane and further cause death. Additionally, the excellent stability in common solvents and good optical stability under UV–visible light facilitated their adsorptive and antibacterial applications.
The transition‐metal‐catalyzed cyclopropanation of alkenes by the decomposition of diazo compounds is a powerful and straightforward strategy to produce cyclopropanes, but is tempered by the ...potentially explosive nature of diazo substrates. Herein we report the Mo‐catalyzed regiospecific deoxygenative cyclopropanation of readily available and bench‐stable 1,2‐dicarbonyl compounds, in which one of the two carbonyl groups acts as a carbene equivalent upon deoxygenation and engages in the subsequent cyclopropanation process. The use of a commercially available Mo catalyst afforded an array of valuable cyclopropanes with exclusive regioselectivity in up to 90 % yield. The synthetic utility of this method was further demonstrated by gram‐scale syntheses, late‐stage functionalization, and the cyclopropanation of a simple monocarbonyl compound. Preliminary mechanistic studies suggest that phosphine (or silane) acts as both a mild reductant and a good oxygen acceptor that efficiently regenerates the catalytically active Mo catalyst through reduction of the Mo‐oxo complexes.
Readily available and bench‐stable 1,2‐dicarbonyl compounds are shown to undergo Mo‐catalyzed regiospecific deoxygenative cyclopropanation. This method has led to an array of valuable cyclopropanes in yields of up to 90 % and with exclusive regioselectivity. This strategy was further applied to the cyclopropanation of a simple monocarbonyl compound.
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