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‘Open access’ is an important part of the open science movement and a significant change to the existing model of academic publication. Based on data from a large-scale survey of Chinese scientists, this paper describes their awareness of, attitudes to and involvement in open access. Policy recommendations on promoting open access in China are proposed at the end of the paper.

At present, most patients with oral squamous cell carcinoma (OSCC) are in the middle or advanced stages at the time of diagnosis. Advanced OSCC patients have a poor prognosis after traditional therapy, and the complex heterogeneity of OSCC has been proven to be one of the main reasons. Single-cell sequencing technology provides a powerful tool for dissecting the heterogeneity of cancer. However, most of the current studies at the single-cell level are static, while the development of cancer is a dynamic process. Thus, understanding the development of cancer from a dynamic perspective and formulating corresponding therapeutic measures for achieving precise treatment are highly necessary, and this is also one of the main study directions in the field of oncology. In this study, we combined the static and dynamic analysis methods based on single-cell RNA-Seq data to comprehensively dissect the complex heterogeneity and evolutionary process of OSCC. Subsequently, for clinical practice, we revealed the association between cancer heterogeneity and the prognosis of patients. More importantly, we pioneered the concept of pseudo-time score of patients, and we quantified the levels of heterogeneity based on the dynamic development process to evaluate the relationship between the score and the survival status at the same stage, finding that it is closely related to the prognostic status. The pseudo-time score of patients could not only reflect the tumor status of patients but also be used as an indicator of the effects of drugs on the patients so that the medication strategy can be adjusted on time. Finally, we identified candidate drugs and proposed precision medication strategies to control the condition of OSCC in two respects: treatment and blocking.

// Haili Wu 1 , Peng Yang 1 , Wanglai Hu 3 , Yingying Wang 1 , Yangxu Lu 4 , Lichao Zhang 1 , Yongsheng Fan 2 , Hong Xiao 5 , Zhuoyu Li 1, 2 1 Institute of Biotechnology, Key Laboratory of Chemical Biology and Molecular Engineering of National Ministry of Education, Shanxi University, Taiyuan 030006, China 2 College of Life Science, Zhejiang Chinese Medical University, Hangzhou 310053, China 3 Department of Immunology, School of Basic Medicine, Anhui Medical University, Hefei 230032, China 4 College of Life Science, Shanxi University, Taiyuan 030006, China 5 The first hospital of Shanxi Medical University, Taiyuan 030006, China Correspondence to: Haili Wu, email: wuhaili0819@163.com Zhuoyu Li, email: lzy@sxu.edu.cn Keywords: PKM2, Drp1, mitochondrial fusion, p53 stability Received: January 28, 2016 Accepted: October 16, 2016 Published: October 27, 2016 ABSTRACT M2-type pyruvate kinase (PKM2) contributes to the Warburg effect. However, it remains unknown as to whether PKM2 has an inhibitory effect on mitochondrial function. We report in this work that PKM2 overexpression inhibits the expression of Drp1 and results in the mitochondrial fusion. The ATP production was found to be decreased, the mtDNA copy number elevated and the expression level of electron transport chain (ETC) complex I, III, V depressed in PKM2 overexpressed cells. PKM2 overexpression showed a decreased p53 protein level and a shorter p53 half-life. In contrast, PKM2 knockdown resulted in increased p53 expression and prolonged half-life of p53. PKM2 could directly bind with both p53 and MDM2 and promote MDM2-mediated p53 ubiquitination. The dimeric PKM2 significantly suppressed p53 expression compared with the other PKM2 mutants. The reverse relationship between PKM2 and Drp1 was further confirmed in a large number of clinical samples. Taken together, the present results highlight a new mechanism that link PKM2 to mitochondrial function, based on p53-Drp1 axis down regulation, revealing a novel therapeutic target in patients with abnormal mitochondria.

Berberine, an isoquinoline alkaloid extracted from coptis, exerts anti-proliferation and anticancer properties. Pyruvate kinase M2 (PKM2) is a key enzyme of aerobic glycolysis and considered as the potential anticancer target. However, the inhibition effects and interaction action between Berberine and PKM2 is not well known. In this study, berberine showed antitumor activity of HCT-116 and HeLa cells with the suppression of cell proliferation. Moreover, berberine inhibited the enzyme activity of PKM2 in cancer cells, but had no impact on PKM2 expression. Further research showed that the interaction between berberine and PKM2 was dynamic fluorescence quenching and the main intermolecular force was hydrogen bonding. These findings revealed that berberine may serve as a therapeutic drug for cancer chemotherapy.

Surgery-induced inflammation has been associated with cancer recurrence and metastasis in colorectal cancer (CRC). As a constituent of gram-negative bacteria, lipopolysaccharide (LPS) is frequently abundant in the peri-operative window. However, the definite roles of LPS in tumour progression remain elusive. Here we reported that LPS treatment increased PKM expression through activation of NF-κB signalling pathway, and knockdown of PKM reversed LPS-induced TNF-α, IL-1β production and cell proliferation in CRC cells. We further showed that the PKM2 but not PKM1 mediated the pro-inflammatory and proliferative effects of LPS. Interestingly, LPS promoted PKM2 binding to the STAT3 promoter to enhance STAT3 expression and its subsequent nuclear translocation. Depletion of STAT3 decreased PKM2-induced TNF-α and IL-1β expression, indicating that STAT3 mediates the pro-inflammatory effects of PKM2. Furthermore, it is the protein kinase activity but not the pyruvate kinase activity of PKM2 that is required for inflammatory cytokine production. Collectively, our findings reveal the NF-κB-PKM2-STAT3 axis as a novel mechanism for the regulation of TNF-α and IL-1β production and suggest the importance of PKM2 as a key inflammatory mediator in inflammatory microenvironment.