Article
Oncology
Yi Gao, Yanfeng Wang, Xiaofei Wang, Changan Zhao, Fenghui Wang, Juan Du, Huahua Zhang, Haiyan Shi, Yun Feng, Dan Li, Jing Yan, Yan Yao, Weihong Hu, Ruxin Ding, Mengjie Zhang, Lumin Wang, Chen Huang, Jing Zhang
Summary: Recent studies have shown that the aberrant expression of miR-335-5p in gastric cancer leads to inhibition of cell proliferation and migration, induction of apoptosis, and arrest of the cell cycle at the G1/S phase through its target gene MAPK10, suggesting that miR-335-5p acts as a tumor suppressor in gastric cancer progression.
CANCER CELL INTERNATIONAL
(2021)
Article
Biotechnology & Applied Microbiology
Jianjie Li, Xiaoyue Xu, Chunhui Liu, Xiaoxue Xi, Yang Wang, Xiaotang Wu, Hua Li
Summary: miR-181a-2-3p promotes GC cell progression by targeting MYLK and enhancing tumor growth. The promoting effect of miR-181a-2-3p on GC cells is reversed when miR-181a-2-3p and MYLK are simultaneously overexpressed.
FRONTIERS IN BIOENGINEERING AND BIOTECHNOLOGY
(2021)
Article
Multidisciplinary Sciences
Soon Auck Hong, Sieun Lee, Jihye Park, Mineui Hong, Jung-Sook Yoon, Heejin Lee, Ji Hyun Lee, Seoree Kim, Hye Sung Won, Keunsoo Kang, Yoon Ho Ko, Young-Ho Ahn
Summary: The study found that miR-199a/b promotes the progression of diffuse gastric cancer (DGC) by targeting FZD6, and can be used as prognostic and diagnostic biomarkers for the disease.
SCIENTIFIC REPORTS
(2023)
Review
Cell Biology
Fang Liu, Yanfen Shi, Zuolong Liu, Ziyi Li, Wei Xu
Summary: Evidence has shown that miRNAs are crucial in the tumorigenesis and progression of various cancers, including gastric cancer, with miR-10a and miR-10b identified as key players in gastric carcinogenesis. Targeting the miR-10 family could be a promising approach for treating gastric cancer, as it regulates multiple aspects of cancer cell behavior and various compounds have shown antitumor activity by targeting these miRNAs.
Article
Cell Biology
Fan Zhang, Guoxian Wang, Wenjuan Yan, Hongmei Jiang
Summary: This study found that miR-4268 is downregulated and KRT80 is upregulated in gastric cancer tissues and cells. Interfering with KRT80 expression inhibits proliferation and migration of gastric cancer cells and promotes apoptosis. MiR-4268 targets KRT80 and negatively regulates its expression, and it may suppress gastric cancer through inhibiting the PI3K/AKT/JNK pathway by targeting KRT80.
Article
Cell Biology
Shanting Gao, Xiaomin Bu, Yongyue Gao, Zengtao Bao, Wenchao Shi, Lipeng Luan, Huiyu Chen, Baoming Zhang, Qingshui Tian, Wenxian Guan, Liuqing Yang
Summary: This study reveals the significant roles of the E2F1-miR-532 double-negative feedback loop in gastric cancer progression. E2F1 is highly upregulated in gastric cancer tissues and correlates with tumor malignancy. MiR-532 is decreased and negatively correlated with E2F1 in gastric cancer tissues. MiR-532 directly targets and inhibits E2F1 expression, affecting proliferation, cell cycle, apoptosis, and DNA damage in gastric cancer cells. Moreover, E2F1 serves as a transcriptional repressor to suppress miR-532 expression, forming a double-negative feedback loop.
CELL DEATH & DISEASE
(2022)
Article
Biochemistry & Molecular Biology
Zhiping Chen, Tianyu Zhong, Tao Li, Jinghua Zhong, Yang Tang, Zhanyu Liu, Baodian Ling, Lanfeng Wang
Summary: The study revealed that SNHG15 exerts oncogenic properties in gastric cancer by targeting miR-506-5p, potentially offering a novel target for GC treatment.
BIOSCIENCE REPORTS
(2021)
Article
Biotechnology & Applied Microbiology
Kun Li, Fengmei Han, Yanping Wu, Xue Wang
Summary: The study identified that miR-340 is highly expressed in retinoblastoma, enhancing cell proliferation, migration, and invasion by regulating WIF1. Moreover, multiple miRNAs and genes were identified that may contribute to a better understanding of the pathogenesis of the disease.
ONCOTARGETS AND THERAPY
(2021)
Article
Multidisciplinary Sciences
Zaibo Zhang, Yong Li, Liqiao Fan, Bingyu Wang, Wenbo Liu, Jiaxiang Cui, Bibo Tan
Summary: This study found that elevated levels of THUMPD3-AS1 in gastric cancer (GC) were associated with poor prognosis. Functionally, THUMPD3-AS1 promoted GC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) and induced tumor growth in vivo. It exerts its regulatory function on BCAT1 through competitive binding with miR-1297.
Article
Multidisciplinary Sciences
Zaibo Zhang, Yong Li, Liqiao Fan, Bingyu Wang, Wenbo Liu, Jiaxiang Cui, Bibo Tan
Summary: This study found that THUMPD3-AS1 is upregulated in gastric cancer and is significantly correlated with poor prognosis. Functionally, THUMPD3-AS1 promotes proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of gastric cancer cells and induces tumor growth in vivo. THUMPD3-AS1 exerts its regulatory function on BCAT1 through competitive binding with miR-1297.
Article
Biotechnology & Applied Microbiology
Hailin Ke, Songling Wu, Yueyi Zhang, Guowei Zhang
Summary: miR-139-3p suppresses gastric cancer by inhibiting the proliferative, migratory, and invasive abilities of GC cells through targeting KIF18B.
Article
Cell Biology
Xuefeng Yang, Shuang Cai, Yue Shu, Xun Deng, Yuanwei Zhang, Nian He, Lei Wan, Xu Chen, Yan Qu, Shouyang Yu
Summary: The study showed an increase in the proportion of M2 macrophages in gastric cancer tissues, where M2 macrophages promoted cell proliferation and tumorigenesis through exosomal miR-487a targeting TIA1. These findings may contribute to the development of novel diagnostic and therapeutic methods for gastric cancer.
Article
Biochemistry & Molecular Biology
Ming Song, Jun Liu, Xin Zheng, Xin Zhou, Zehui Feng, Wei Hu
Summary: The study found that the expression of CEMIP was significantly elevated while miR-148a-3p level was downregulated in gastric cancer tissues and cell lines. miR-148a-3p suppressed the development of gastric cancer by inhibiting the expression of CEMIP.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2021)
Article
Cell Biology
Zihao Chen, Yong Li, Bibo Tan, Fang Li, Qun Zhao, Liqiao Fan, Zhidong Zhang, Xuefeng Zhao, Yu Liu, Dong Wang
Summary: This study revealed that Lnc_ASNR is highly expressed in gastric cancer and promotes cell proliferation, migration, and invasion by regulating the miR-519e-5p/FGFR2 pathway. Lnc_ASNR functions as a ceRNA targeting miR-519e-5p, and its effects are closely related to epithelial-mesenchymal transition (EMT) in gastric cancer development.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Oncology
Ling Gao, Tingting Xia, Mingde Qin, Xiaofeng Xue, Linhua Jiang, Xinguo Zhu
Summary: The study reveals that circPTK2 functions as a tumor suppressor in gastric cancer by regulating the miR-196a-3p/AATK axis, leading to the suppression of cancer cell proliferation, migration, and invasion. This suggests that circPTK2 may serve as a novel therapeutic target for gastric cancer.
FRONTIERS IN ONCOLOGY
(2021)
Article
Environmental Sciences
Jian Lu, Yun Yang, Lianhua Zhu, Meng Li, Wenping Xu, Cheng Zhang, Jiagao Cheng, Liming Tao, Zhong Li, Yang Zhang
Summary: Natural pyrethrins induce oxidative stress, DNA damage and liver toxicity in both human HepG2 cells and zebrafish. The observed chronic toxicity may lead to irreversible DNA damage and severe toxic effects on cells. In conclusion, hepatotoxicity of natural pyrethrins poses a risk to human health by causing liver degeneration and steatosis.
Editorial Material
Multidisciplinary Sciences
Jiaojiao Ni, Mingchun Jiang, Yanyan Chen, Xianping Rao, Junjie Jiang, Zizhen Zhang, Fangyu Ju, Dongyang Guo, Boya Wang, Lisong Teng, Liangjing Wang, Tianhua Zhou, Wei Zhuo
Article
Engineering, Biomedical
Huifang Wang, Haoyu Bai, Jiafeng Wang, Xuefei Zhou, Hongda Chen, Liying Wang, Huiming Ren, Zimo Liu, Wei Zhuo, Zhuxian Zhou, Jianbin Tang, Zhijie Li, Jigang Wang, Youqing Shen, Tianhua Zhou, Xiangrui Liu
Summary: Effective combination therapies are urgently needed for the treatment of triple-negative breast cancer (TNBC). In this study, researchers found that the autophagy inhibitor hydroxychloroquine (HCQ) and the topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin (SN38) exhibit synergistic effects when combined at a specific molar ratio. They further developed a glutathione-responsive self-assembled combination nanoparticle (Combo NP) that integrates the two drugs at the optimized ratio. In TNBC cells, the Combo NP significantly enhanced the cytotoxic effects of SN38 by blocking autophagy, leading to improved therapeutic benefit in metastatic TNBC models.
Editorial Material
Cell Biology
Yong Tang, Yibin Kang
Summary: The study found that the microbial metabolite TMAO enhances CD8(+) T cell-mediated antitumor immunity in triple-negative breast cancer (TNBC) by inducing pyroptosis in tumor cells, thus improving the efficacy of immunotherapy.
Review
Biochemistry & Molecular Biology
Xiying Chen, Zhouyuanjing Shi, Feng Yang, Tianhua Zhou, Shanshan Xie
Summary: Cilia are microtubule-based organelles that play crucial roles in cellular signaling pathways and extracellular fluid movement. Defects in ciliary structures and functions are implicated in hereditary disorders known as ciliopathies. Proteomic studies provide important clues for understanding the physiological and pathological roles of cilia.
Article
Multidisciplinary Sciences
Shujie Chen, Lu Zhang, Mengjie Li, Ying Zhang, Meng Sun, Lingfang Wang, Jiebo Lin, Yun Cui, Qian Chen, Chenqi Jin, Xiang Li, Boya Wang, Hao Chen, Tianhua Zhou, Liangjing Wang, Chih-Hung Hsu, Wei Zhuo
Summary: The study reveals that Fusobacterium nucleatum contributes to colorectal cancer (CRC) progression by reducing global m(6)A modifications through a YAP/FOXD3/METTL3/KIF26B axis. Fusobacterium nucleatum is closely associated with the development of CRC.
NATURE COMMUNICATIONS
(2022)
Article
Cell Biology
Jingjing Meng, Yi-zhou Jiang, Shen Zhao, Yuwei Tao, Tengjiang Zhang, Xuxiang Wang, Yuan Zhang, Keyong Sun, Min Yuan, Jin Chen, Yong Wei, Xun Lan, Mo Chen, Charles J. David, Zhijie Chang, Xiaohuan Guo, Deng Pan, Meng Chen, Zhi-Ming Shao, Yibin Kang, Hanqiu Zheng
Summary: This study reveals that Jagged1, derived from tumors, plays a crucial role in regulating the immune microenvironment of breast cancer. Jagged1 promotes tumorigenesis and facilitates the recruitment of macrophages into the tumor microenvironment by activating the Notch pathway. Educated macrophages then interact with tumor-infiltrating T cells to inhibit their proliferation and tumoricidal activity. The high expression of Jagged1 in triple-negative breast cancer patients is associated with increased macrophage infiltration and decreased T cell activity. Co-administration of an ICI PD-1 antibody with a Notch inhibitor effectively inhibits tumor growth in breast cancer models, suggesting potential therapeutic targets.
Article
Cell Biology
Wenjun Kuang, Hao Jin, Feng Yang, Xiying Chen, Jianzhao Liu, Ting Li, Yongxia Chang, Min Liu, Zhangqi Xu, Chunxiao Huo, Xiaoyi Yan, Yuehong Yang, Wei Liu, Qiang Shu, Shanshan Xie, Tianhua Zhou
Summary: The study reveals that the m(1)A demethylase ALKBH3 inhibits ciliogenesis by removing m(1)A sites on Aurora A mRNA. Depletion of ALKBH3 leads to ciliary defects in zebrafish embryos, which can be rescued by wild-type ALKBH3. These findings highlight the crucial role of ALKBH3-dependent m(1)A demethylation in ciliogenesis and developmental events.
Article
Cell Biology
Wei Zhuo, Meng Sun, Kun Wang, Lu Zhang, Kai Li, Danyang Yi, Mengjie Li, Qiang Sun, Xixi Ma, Wei Liu, Lisong Teng, Chengqi Yi, Tianhua Zhou
Summary: This study reveals the significance of PCIF1 and m(6)Am modification in gastric cancer. Increased expression of PCIF1 and m(6)Am modification are associated with gastric cancer progression and poor prognosis. Silencing PCIF1 inhibits the proliferation and invasion of gastric cancer cells, and suppresses tumor growth and metastasis in a mouse model. PCIF1 modifies TM9SF1 mRNA with m(6)Am, leading to decreased TM9SF1 translation. TM9SF1 reverses the effects of PCIF1 on gastric cancer cell aggressiveness.
Article
Multidisciplinary Sciences
Tao Wan, Jiafeng Zhong, Qi Pan, Tianhua Zhou, Yuan Ping, Xiangrui Liu
Summary: CRISPR-Cas9 gene editing is a powerful therapeutic technology, but the lack of safe and efficient in vivo delivery systems limits its clinical applications. Researchers have developed a novel gene editing delivery system, called exosomeRNP, which loads Cas9 RNPs into purified exosomes derived from hepatic stellate cells. exosomeRNP enables effective cytosolic delivery of RNPs in vitro and specifically accumulates in liver tissue in vivo. By targeting different genes, exosomeRNP demonstrates considerable therapeutic potential in acute liver injury, chronic liver fibrosis, and hepatocellular carcinoma mouse models. This study provides a feasible platform for precise and tissue-specific gene therapies for liver diseases.
Article
Oncology
Chengheng Liao, Xijuan Liu, Cheng Zhang, Qing Zhang
Summary: Hypoxia, characterized by diminished oxygen availability, has a significant impact on the tumor microenvironment, leading to abnormal vasculature, altered metabolism, and immune suppression. Limited effectiveness and development of resistance to anti-tumor therapy are also associated with hypoxia in the tumor microenvironment. This review summarizes the molecular mechanisms underlying hypoxic cellular responses and adaptations, and emphasizes the effects of hypoxia on angiogenesis, cellular metabolism, and immune suppression within the tumor microenvironment. Additionally, the recent advances in targeting hypoxia for therapeutic implications are discussed. A comprehensive understanding of hypoxia and its role in tumors will contribute to the development of improved cancer treatments.
SEMINARS IN CANCER BIOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Wei Wan, Chuying Qian, Qian Wang, Jin Li, Hongtao Zhang, Lei Wang, Maomao Pu, Yewei Huang, Zhengfu He, Tianhua Zhou, Han-Ming Shen, Wei Liu
Summary: The cGAS-STING pathway plays a crucial role in host defense by sensing pathogen DNA and inducing immune responses. In this study, it was discovered that STING directly interacts with WIPI2, a key protein involved in autophagy. This interaction is necessary for the formation of autophagosomes induced by STING, but does not affect the activation and trafficking of STING. Furthermore, the specific interaction between STING and WIPI2 leads to competition with PI3P binding, resulting in mutual inhibition between STING-induced autophagy and canonical PI3P-dependent autophagy.
Review
Oncology
Minhong Shen, Yibin Kang
Summary: The traditional approach to cancer therapeutics targets driver oncogenes, but this method has limitations such as toxicity to normal tissue and treatment resistance. However, a new class of genes called 'cancer fitness genes' have been identified, which play crucial roles in metastasis. These genes help tumor cells adapt to changing microenvironments, facilitating tumor progression and metastasis. They have therapeutic potential as targeting them is less likely to harm noncancerous tissues.
Article
Oncology
Minhong Shen, Yong Wei, Hahn Kim, Liling Wan, Yi-Zhou Jiang, Xiang Hang, Michael Raba, Stacy Remiszewski, Michelle Rowicki, Cheng-Guo Wu, Songyang Wu, Lanjing Zhang, Xin Lu, Min Yuan, Heath A. Smith, Aiping Zheng, Joseph Bertino, John F. Jin, Yongna Xing, Zhi-Ming Shao, Yibin Kang
Summary: Targeting the MTDH-SND1 complex shows significant therapeutic potential for metastatic breast cancer. Specific compounds C26-A2 and C26-A6 inhibit tumor growth and metastasis, as well as enhancing chemotherapy sensitivity.
Article
Oncology
Minhong Shen, Heath A. Smith, Yong Wei, Yi-Zhou Jiang, Sheng Zhao, Nicole Wang, Michelle Rowicki, Yong Tang, Xiang Hang, Songyang Wu, Liling Wan, Zhi-Ming Shao, Yibin Kang
Summary: By targeting the MTDH-SND1 interaction through genetic and pharmacological approaches, it has been found that the complex plays a crucial role in suppressing antitumor T cell responses in breast cancer, ultimately enhancing immune surveillance and sensitivity to anti-programmed cell death protein 1 therapy. This suggests that combination therapy could be a viable approach to increase immune-checkpoint blockade therapy responses in metastatic breast cancer, providing a potential new strategy for treatment.
Review
Oncology
Xinru Zhou, Yin Jia, Chuanbin Mao, Shanrong Liu
Summary: Small extracellular vesicles (sEVs), such as exosomes, have emerged as crucial targets for liquid biopsy and promising drug delivery vehicles in tumor progression. They can serve as biomarkers for tumor diagnosis and as drug carriers for cancer treatment.
Article
Oncology
Ruochan Chen, Ju Zhu, Xiao Zhong, Jie Li, Rui Kang, Daolin Tang
Summary: The interplay between autophagy and apoptosis plays a crucial role in tumorigenesis and cancer therapy, with HMGB1 serving as a key regulator in these processes.
Article
Oncology
Zongfu Pan, Xixuan Lu, Tong Xu, Jinming Chen, Lisha Bao, Ying Li, Yingying Gong, Yulu Che, Xiaozhou Zou, Zhuo Tan, Ping Huang, Minghua Ge
Summary: This study uncovered the emerging role of HN1 in promoting dedifferentiation of anaplastic thyroid cancer (ATC) cells. HN1 negatively regulated the thyroid differentiation markers and had an inhibitory effect on the transcriptional activation of CTCF, thereby influencing the chromatin accessibility of thyroid differentiation genes.
Article
Oncology
Yi Qin, Shengjun Xiong, Jun Ren, Gautam Sethi
Summary: Autophagy plays an important regulatory role in glioblastoma, and its dysregulation can lead to drug resistance and radioresistance. It also affects stem cell characteristics, overall growth, and metastasis. Therefore, autophagy is a promising target for glioblastoma therapy.
Article
Oncology
Katsuya Nagaoka, Xuewei Bai, Dan Liu, Kevin Cao, Joud Mulla, Chengcheng Ji, Hongze Chen, Muhammad Azhar Nisar, Amalia Bay, William Mueller, Grace Hildebrand, Jin-Song Gao, Shaolei Lu, Hiroko Setoyama, Yasuhito Tanaka, Jack R. Wands, Chiung-Kuei Huang
Summary: This study found that serum 2-OG levels in cholangiocarcinoma patients are associated with the effectiveness of chemotherapy. Patients with progressive disease showed significantly higher levels of serum 2-OG compared to stable disease and partial response patients. The study also revealed that overexpression of ASPH mimics the effects of 2-OG, and knockdown of ASPH improves chemotherapy. Targeting ASPH enhances the effects of chemotherapy by modulating ATM and ATR, two key regulators of DDRs.
