Latest Issue
Issue 2 ， 2022
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Autophagy and cancer treatment: four functional forms of autophagy and their therapeutic applications
Abstract：Cancer is the leading cause of death worldwide. Drugs play a pivotal role in cancer treatment, but the complex biological processes of cancer cells seriously limit the efficacy of various anticancer drugs. Autophagy, a self-degradative system that maintains cellular homeostasis, universally operates under normal and stress conditions in cancer cells. The roles of autophagy in cancer treatment are still controversial because both stimulation and inhibition of autophagy have been reported to enhance the effects of anticancer drugs. Thus, the important question arises as to whether we should try to strengthen or suppress autophagy during cancer therapy. Currently, autophagy can be divided into four main forms according to its different functions during cancer treatment: cytoprotective (cell survival), cytotoxic (cell death), cytostatic (growth arrest), and nonprotective (no contribution to cell death or survival). In addition, various cell death modes, such as apoptosis, necrosis, ferroptosis, senescence, and mitotic catastrophe, all contribute to the anticancer effects of drugs. The interaction between autophagy and these cell death modes is complex and can lead to anticancer drugs having different or even completely opposite effects on treatment. Therefore, it is important to understand the underlying contexts in which autophagy inhibition or activation will be beneficial or detrimental. That is, appropriate therapeutic strategies should be adopted in light of the different functions of autophagy. This review provides an overview of recent insights into the evolving relationship between autophagy and cancer treatment.Keywords：Autophagy;Cancer treatment;Precision treatment;Cell death mode- 166
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Published：2022-03-07 -
Molecular hydrogen is a promising therapeutic agent for pulmonary disease
Abstract：Molecular hydrogen exerts biological effects on nearly all organs. It has anti-oxidative, anti-inflammatory, and anti-aging effects and contributes to the regulation of autophagy and cell death. As the primary organ for gas exchange, the lungs are constantly exposed to various harmful environmental irritants. Short- or long-term exposure to these harmful substances often results in lung injury, causing respiratory and lung diseases. Acute and chronic respiratory diseases have high rates of morbidity and mortality and have become a major public health concern worldwide. For example, coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global pandemic. An increasing number of studies have revealed that hydrogen may protect the lungs from diverse diseases, including acute lung injury, chronic obstructive pulmonary disease, asthma, lung cancer, pulmonary arterial hypertension, and pulmonary fibrosis. In this review, we highlight the multiple functions of hydrogen and the mechanisms underlying its protective effects in various lung diseases, with a focus on its roles in disease pathogenesis and clinical significance.Keywords：Molecular hydrogen;Pulmonary disease;Reactive oxygen species (ROS);Oxidative stress;Inflammation- 86
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Published：2022-03-07 -
Index of microcirculatory resistance: state-of-the-art and potential applications in computational simulation of coronary artery disease
Abstract：The dysfunction of coronary microcirculation is an important cause of coronary artery disease (CAD). The index of microcirculatory resistance (IMR) is a quantitative evaluation of coronary microcirculatory function, which provides a significant reference for the prediction, diagnosis, treatment, and prognosis of CAD. IMR also plays a key role in investigating the interaction between epicardial and microcirculatory dysfunctions, and is closely associated with coronary hemodynamic parameters such as flow rate, distal coronary pressure, and aortic pressure, which have been widely applied in computational studies of CAD. However, there is currently a lack of consensus across studies on the normal and pathological ranges of IMR. The relationships between IMR and coronary hemodynamic parameters have not been accurately quantified, which limits the application of IMR in computational CAD studies. In this paper, we discuss the research gaps between IMR and its potential applications in the computational simulation of CAD. Computational simulation based on the combination of IMR and other hemodynamic parameters is a promising technology to improve the diagnosis and guide clinical trials of CAD.Keywords：Index of microcirculatory resistance (IMR);Coronary artery disease (CAD);Computational simulation- 178
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Published：2022-03-07
Review
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A high-efficiency and versatile CRISPR/Cas9-mediated HDR-based biallelic editing system
Abstract：Clustered regulatory interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 nuclease (Cas9), the third-generation genome editing tool, has been favored because of its high efficiency and clear system composition. In this technology, the introduced double-strand breaks (DSBs) are mainly repaired by non-homologous end joining (NHEJ) or homology-directed repair (HDR) pathways. The high-fidelity HDR pathway is used for genome modification, which can introduce artificially controllable insertions, deletions, or substitutions carried by the donor templates. Although high-level knock-out can be easily achieved by NHEJ, accurate HDR-mediated knock-in remains a technical challenge. In most circumstances, although both alleles are broken by endonucleases, only one can be repaired by HDR, and the other one is usually recombined by NHEJ. For gene function studies or disease model establishment, biallelic editing to generate homozygous cell lines and homozygotes is needed to ensure consistent phenotypes. Thus, there is an urgent need for an efficient biallelic editing system. Here, we developed three pairs of integrated selection systems, where each of the two selection cassettes contained one drug-screening gene and one fluorescent marker. Flanked by homologous arms containing the mutated sequences, the selection cassettes were integrated into the target site, mediated by CRISPR/Cas9-induced HDR. Positively targeted cell clones were massively enriched by fluorescent microscopy after screening for drug resistance. We tested this novel method on the amyloid precursor protein (APP) and presenilin 1 (PSEN1) loci and demonstrated up to 82.0% biallelic editing efficiency after optimization. Our results indicate that this strategy can provide a new efficient approach for biallelic editing and lay a foundation for establishment of an easier and more efficient disease model.Keywords：Biallelic editing;CRISPR/Cas9;Homology-directed repair (HDR);Homozygote- 154
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Published：2022-03-07
Research Article
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Analysis of volatile organic compounds in exhaled breath after radiotherapy
Abstract：放射治疗具有一定风险，主要是因为其在杀死癌细胞的同时可对正常细胞造成严重损伤。呼气中的挥发性有机化合物（VOCs）可以提供人体内生理以及病理相关过程的信息，具有监测机体损伤的潜力。本研究收集了10名肺癌患者的110份呼气样本，使用固相微萃取气相色谱-质谱技术（SPME-GC/MS）进行检测。通过热图分析可发现28种VOCs（包括芳香族化合物、烷烃、醛类、酸类、酮类、醇类和酯类）在放疗后6小时内发生规律性的变化。通过对放疗前后0.5小时的呼气样本进行Mann-Whitney U检验和正交偏最小二乘判别分析（OPLS-DA），丙酸、三乙酸甘油酯和吲哚可被确定为放疗的呼气标志物。所建立的OPLS-DA模型的预测优度参数Q2为0.53，显示出良好的预测能力。综上所述，呼气VOCs可用于监测放射治疗造成的机体损伤，有助于制定个体化治疗方案。Keywords：放射治疗;呼气;挥发性有机物;气相色谱质谱;生物标志物- 24
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Published：2022-03-07 -
Upregulation of h-TERT and Ki-67 in ectopic endometrium is associated with recurrence of endometriosis
Abstract：目的：探讨人类端粒酶逆转录酶（h-TERT）和Ki-67与子宫内膜异位症复发的相关性。创新点：第一次将h-TERT和Ki-67联合表达水平可作为卵巢子宫内膜异位症复发的有用预测标志物。方法：收集30例术后30个月复发的卵巢子宫内膜异位症患者、30例术后30个月未复发的卵巢子宫内膜异位症患者和30例对照组的子宫内膜异位症组织样本。采用免疫组织化学方法检测异位子宫内膜组织中h-TERT和Ki-67的表达。结论：h-TERT和Ki-67联合表达水平可作为卵巢子宫内膜异位症复发的有用预测标志物，子宫内膜h-TERT过度表达以及术后血清CA125水平升高可能在卵巢子宫内膜异位症复发中起重要作用。Keywords：卵巢子宫内膜异位症;复发;人端粒酶逆转录酶（h-TERT）;Ki-67;CA125- 117
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Published：2022-03-07 -
Chemerin promotes proliferation and migration of ovarian cancer cells by upregulating expression of PD-L1
Abstract：目的：探究腹腔肿瘤微环境内脂肪因子趋化素（chemerin）与程序性死亡配体-1（PD-L1）是否存在关联，及其对卵巢癌细胞系HO8910细胞生物学功能的影响。创新点：首次发现了chemerin可以上调卵巢癌细胞PD-L1的表达，促进肿瘤增殖和迁移。这对进一步研究免疫抑制剂在卵巢癌治疗中的应用、卵巢癌的早期诊断，以及血清和腹水中chemerin的检测具有一定的指导意义。此外，chemerin结合其他脂肪因子是否能成为卵巢癌诊断的标志物，需进一步的研究证实。方法：使用酶联免疫吸附剂测定（ELISA）检测卵巢癌患者腹水和血清中chemerin的含量；使用免疫组化检测卵巢癌肿瘤组织中chemerin和PD-L1的表达；使用免疫印迹法检测卵巢癌组织中PD-L1的表达及在HO8910和HO891PM细胞中chemerin表达的差异；利用浓度分别为0、10、50和100 ng/mL外源性chemerin刺激HO8910和HO8910PM细胞；使用水溶性四唑（WST）检测细胞增殖；使用划痕实验检测细胞迁移功能；利用鬼笔环肽荧光染色在共聚焦显微镜下观察PD-L1敲除前后的HO8910和HO8910PM的细胞骨架变化；使用免疫印迹法检测细胞骨架蛋白的表达情况。结论：Chemerin可以上调卵巢癌细胞PD-L1的表达，对肿瘤增殖和迁移具有促进作用。Keywords：卵巢癌;腹腔肿瘤微环境;脂肪因子;程序性死亡配体-1（PD-L1）- 27
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Published：2022-03-07
Correspondence
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Erratum to: Inhibition of chemotherapy-related breast tumor EMT by application of redox-sensitive siRNA delivery system CSO-ss-SA/siRNA along with doxorubicin treatment
Abstract：The online version of the original article can be found at https://doi.org/10.1631/jzus.B1900468The original version of this article (Liu et al., 2020) unfortunately contained some mistakes.1. Figs. 7c and 7d in p.229 were incorrect. The upper left and bottom left pictures in Fig. 7c were accidentally duplicated with the pictures at the same position of Fig. 1a. The upper right and bottom right pictures were mistakenly placed in Fig. 7c. Therefore, the calculation results in Fig. 7d were also mistaken. The correct versions should be as follows:2. Because of the wrong pictures of Fig. 7c, the calculated results of "42.5%" in Abstract, Sections 3.9 and 5 are also mistaken. The correct result should be "45.2%."(1) Lines 10–12 of Abstract in p.218: "CSO-ss-SA/siRNA could effectively transmit siRNA into tumor cells, reducing the expression of RAC1 protein by 38.2% and decreasing the number of tumor-induced invasion cells by 42.5%." was incorrect. The correct version should be "CSO-ss-SA/siRNA could effectively transmit siRNA into tumor cells, reducing the expression of RAC1 protein by 38.2% and decreasing the number of tumor-induced invasion cells by 45.2%."(2) Lines 23–26 of Section 3.9 in p.227: "It was shown that the number of invasive tumor cells induced by DOX was reduced by 42.5% since CSO-ss-SA/siRNA downregulated the expression of RAC1 protein." was incorrect. The correct version should be "It was shown that the number of invasive tumor cells induced by DOX was reduced by 45.2% since CSO-ss-SA/siRNA downregulated the expression of RAC1 protein."(3) Lines 4–8 of Section 5 in p.231: "CSO-ss-SA, as an efficient redox-sensitive carrier for delivering siRNA silencing RAC1 into tumor cells, reduced the expression of RAC1 by 38.2% and decreased DOX-induced tumor invasion cells by 42.5% in vitro." was incorrect. The correct version should be "CSO-ss-SA, as an efficient redox-sensitive carrier for delivering siRNA silencing RAC1 into tumor cells, reduced the expression of RAC1 by 38.2% and decreased DOX-induced tumor invasion cells by 45.2% in vitro."- 15
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Published：2022-03-07
Erratum
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