Central environmental protection inspections have completed their goal of full coverage of 31 provinces in China, and more than 17,000 officials have been held accountable. The media has evaluated the effectiveness of central environmental protection inspections using the notions of “instant results” and the “miracle drug of environmental governance.” Can this approach effectively promote local environmental governance? This paper takes the treatment effect of central environmental protection inspections on air pollution as an example. Using the method of regression discontinuity, central environmental protection inspections are found to have a positive effect on the air quality index (AQI), but this effect is only short term and unsustainable. Additionally, there are inter-provincial differences. Judging from the research results on sub-contaminants, the treatment effect of central environmental protection inspections on air pollution is mainly reflected in PM10, PM2.5 and CO. Under the current situation in which PM10 and PM2.5 are the main assessment indexes, this phenomenon indicates that due to the political achievements and promotion of local officials and for reasons of accountability, it is more effective for the central government to conduct specific environmental assessments through local governments than to conduct central environmental protection inspections.

Uncontrolled proliferation is the hallmark of cancer cells. Previous studies mainly focused on the role of protein-coding genes in cancer cell proliferation. Emerging evidence showed that long non-coding RNAs (lncRNAs) also play critical roles in cancer cell proliferation and growth. LncRNA KCNQ1OT1 is found to contribute to carcinogenesis, but its role in acute promyelocytic leukemia (APL) is unclear. In this study, by analyzing data from Gene Expression Omnibus, The Cancer Genome Atlas database and our clinical samples, we found that KCNQ1OT1 was selectively highly expressed in APL. Functional assays demonstrated that knockdown of KCNQ1OT1 reduced APL cell proliferation and increased apoptosis. Further evidence showed that KCNQ1OT1 was mainly located in the cytoplasm of APL patient-derived NB4 cells and APL patient bone marrow samples. Mechanistically, KCNQ1OT1 bound to RNA binding protein FUS, and silencing either KCNQ1OT1 or FUS reduced the expression level and stability of MAP3K1 mRNA. Whereas KCNQ1OT1 and FUS did not affect each other. Importantly, knockdown of MAP3K1 impaired APL cell proliferation. Finally, c-Myc transactivated KCNQ1OT1 in APL cells through binding to its promoter while knockdown of c-Myc decreased KCNQ1OT1 expression. Our results not only revealed that c-Myc transactivated KCNQ1OT1 and upregulated KCNQ1OT1 promoted APL cell proliferation, but also demonstrated that KCNQ1OT1 bound to FUS to synergistically stabilize MAP3K1 mRNA, thus facilitating APL cell proliferation. This study established a previously unidentified role of KCNQ1OT1 in the development of APL, and KCNQ1OT1 may serve as a potential therapeutic target for APL.

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