ABSTRACT
Driving enterprises to implement carbon emission reduction actions and reduce carbon emissions is a crucial research topic in achieving the carbon peaking and carbon neutrality goals. As a significant external environment factor influencing corporate behavior, can institutional pressures effectively promote enterprises to reduce carbon emissions? This study aims to probe into the impact and mechanism of three institutional pressures, namely coercive, mimetic, and normative, on corporate carbon emissions, taking Chinese-listed companies as the research object. The results indicate that coercive pressure is positively associated with corporate carbon reduction, while normative pressure has no significant impact. Furthermore, mimetic pressure impedes corporate carbon emissions. The mechanism test shows that carbon reduction is a mediator in the influence exerted by three institutional pressures on corporate carbon emissions. In response to coercive pressure and mimetic pressure, enterprises tend to reduce their carbon emissions by cultivating concepts related to carbon emission reduction. Concepts related to carbon reduction play a more dominant role than carbon reduction actions when both are mediators, with the former even replacing the latter. This research provides a new perspective for improving corporate environmental performance and corporate sustainability.
Subject(s)
Carbon , China , Health Facilities , Organizations , Social ConditionsABSTRACT
Mounting literatures have revealed the crucial effects of long noncoding RNA (lncRNA) in various cancers, including glioma. HNF1A-AS1, a novel lncRNA, is reported to modulate tumorigenesis and development of multiple cancers. However, the tumorigenic function of lncRNA HNF1A-AS1 in glioma remains largely unknown. quantitative reverse transcription and polymerase chain reaction and western blot assays were applied to evaluate the expression of relevant mRNAs and proteins. 5-Ethynyl-2'- deoxyuridine, terminal deoxynucleotidyl transferase dUTP nick-end labeling, flow cytometry, and transwell assays were conducted for examining the influence of HNF1A-AS1 on glioma cell functions. The relationship among RNAs was investigated by mechanical experiments. The results demonstrated that HNF1A-AS1 was predominantly highly expressed in glioma cell lines compared with nontumor glial epithelial cell, which was associated with the stimulation of transcription factor myelocytomatosis oncogene. Knockdown of HNF1A-AS1 remarkably inhibited glioma cells proliferation, migration, and invasion, while accelerating cell apoptosis in vitro. Mechanically, HNF1A-AS1 served as a miR-32-5p sponge. Moreover, SOX4 was discovered as a target of miR-32-5p. Inhibited miR-32-5p or upregulated SOX4 could markedly counteract the inhibitory effects of silencing HNF1A-AS1 on glioma malignant biological behaviors. HNF1A-AS1 exerted oncogenic property in glioma progression via upregulating miR-32-5p-mediated SOX4 expression, suggesting potential novel therapeutic target for future glioma treatment.
Subject(s)
Brain Neoplasms/metabolism , Glioma/metabolism , MicroRNAs/metabolism , Proto-Oncogene Proteins c-myc/metabolism , RNA, Long Noncoding/metabolism , SOXC Transcription Factors/metabolism , Animals , Apoptosis , Brain Neoplasms/etiology , Brain Neoplasms/pathology , Cell Line, Tumor , DNA Nucleotidylexotransferase , Deoxyuridine/analogs & derivatives , Disease Progression , Flow Cytometry , Gene Silencing , Glioma/etiology , Glioma/pathology , Humans , In Situ Nick-End Labeling , Male , Mice , Mice, Nude , Neoplasm Proteins/metabolism , RNA, Long Noncoding/genetics , Transcription Factors/metabolismABSTRACT
Expression of IL-1 and proteasome are elevated in burned animals and patients. However, whether the increased level of IL-1 correlates with the increased activity and expression of 26S proteasome after burn has not been studied. In the present study, we investigated the role of single IL-1 factor on activation of the 26S proteasome first by injection of recombinant IL-1 into the normal rats. Results indicated that proteolytic activity and the expression of the 26S proteasome increased remarkably 24 and 48 h after-IL-1 injection, respectively. We then studied the potential role of IL-1 on activity and expression of the proteasome in the burned rat by using neutralizing monoclonal antibody against IL-1. Results demonstrated that activity and the expression of 26S proteasome were decreased partially but significantly 48 h after-burn when circulating IL-1 in injured animals was neutralized. These results indicate that IL-1 may play a key role on the activity and expression of 26S proteasome following burn. The proteasome has been verified as being deeply involved in the mechanism of accelerated muscle protein breakdown after burn, these results imply that IL-1 might be involved in the protein metabolism after-burn by activating the proteasome pathway, though protein metabolism directly affected by IL-1 had not been assessed in this study.
