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428 results on '"Song, Yongmei"'

2. Genomic characterization and risk stratification of esophageal squamous dysplasia

Author

Min Qingjie, Zhang Min, Lin Dongmei, Zhang Weimin, Li Xianfeng, Zhao Lianmei, Teng Huajing, He Tao, Sun Wei, Fan Jiawen, Yu Xiying, Chen Jie, Li Jinting, Gao Xiaohan, Dong Bin, Liu Rui, Liu Xuefeng, Song Yongmei, Cui Yongping, Lu Shih-Hsin, Li Ruiqiang, Guo Mingzhou, Wang Yan, and Zhan Qimin

Subjects
esophageal squamous dysplasia, genomic alteration, acsm5, early diagnosis, mir-4292, Medicine
Abstract

The majority of esophageal squamous dysplasia (ESD) patients progress slowly, while a subset of patients can undergo recurrence rapidly or progress to invasive cancer even after proper treatment. However, the molecular mechanisms underlying these clinical observations are still largely unknown.

Published
2024
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11. Corrigendum to “Spatially resolved metabolomics combined with multicellular tumor spheroids to discover cancer tissue relevant metabolic signatures” [Anal. Chim. Acta 1155 (2021) 338342]

Author

Zang, Qingce, primary, Sun, Chenglong, additional, Chu, Xiaoping, additional, Li, Limei, additional, Gan, Wenqiang, additional, Zhao, Zitong, additional, Song, Yongmei, additional, He, Jiuming, additional, Zhang, Ruiping, additional, and Abliz, Zeper, additional

Published
2024
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12. PTBP1 promotes IRES-mediated translation of cyclin B1in cancer

Author

Fan Xinyi, Zhao Zitong, Ma Liying, Huang Xuanlin, Zhan Qimin, and Song Yongmei

Subjects
cyclin B1, internal ribosome entry site, PTBP1, interacting trans-acting factors, esophageal squamous cell carcinoma, Biochemistry, QD415-436, Genetics, QH426-470
Abstract

Cyclin B1 is an essential cyclin-dependent protein that involves in the G2/M transition. Multiple studies report that cyclin B1 is upregulated in cancers and promotes cancer progression. However, the mechanism of cyclin B1 upregulation remains unclear. Here we report that the 5′UTR of cyclin B1 mRNA contains an internal ribosome entry site (IRES) by using a bicistronic fluorescent reporter. We show that IRES can initiate the translation of cyclin B1, and the IRES-mediated translation is further activated under cell stress. Interacting trans-acting factors (ITAFs) are required by most IRES to initiate the translation. We find that PTBP1 promotes the IRES-mediated translation of cyclin B1 by binding to the 5′UTR of cyclin B1. On top of that, PTBP1 promotes the malignancy of ESCC cells. Our data suggest that the IRES-mediated translation of cyclin B1 plays an essential role in the cyclin B1 upregulation in cancers.

Published
2022
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19. Research progress on fusion genes in tumours.

Author

Chang, Yinyi, Zhao, Zitong, and Song, Yongmei

Subjects
GENE fusion, GENE therapy, TUMORS, GENE targeting
Abstract

Background: The concept of gene fusion describes the process of fusing two genes into one, which is closely linked to tumour occurrence and development and may even be the direct cause of some tumours. Due to their tumour‐specific expression and ability to drive tumour occurrence and development, there is great potential for fusion genes to be used as diagnostic markers and targets for specific types of tumours. Main body: Although many fusion genes have been detected so far, they mainly focus on a small number of highly recurrent fusion genes detected in patients' tumours. There are few studies on the functional mechanism and clinical relevance of rare gene fusions. Our review discusses the generation mechanisms, detection methods, biological functions, and mechanisms of action of fusion genes. Additionally, we discuss the clinical significance of fusion gene detection in some tumour types. Conclusion: The function mechanism research of rare gene fusion is very necessary, and more functions of fusion genes independent of unfused/normal genes can be explored in future studies. There is still a long way to go in implementing precision tumour therapy targeting gene fusion. [ABSTRACT FROM AUTHOR]

Published
2024
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26. CircMALAT1 promotes cancer stem‐like properties and chemoresistance via regulating Musashi‐2/c‐Myc axis in esophageal squamous cell carcinoma.

Author

Zhao, Zitong, Deng, Yingni, Han, Jing, Ma, Liying, Zhu, Yumeng, Zhang, Hua, He, Zhixu, and Song, Yongmei

Subjects
SQUAMOUS cell carcinoma, ESOPHAGEAL cancer, RNA-binding proteins, DRUG resistance in cancer cells, CANCER stem cells, DRUG resistance
Abstract

The primary challenge in treating esophageal squamous cell carcinoma (ESCC) is resistance to chemotherapy. Cancer stem cell (CSC) is the root cause of tumor drug resistance. Therefore, targeting CSCs has been considered promising therapeutic strategy for tumor treatment. Here, we report that circMALAT1 was significantly upregulated in ESCC CSC‐like cells and primary tumors from ESCC patients. Clinically, there was a positive correlation between circMALAT1 expression and ESCC stage and lymph node metastasis, as well as poor prognosis for ESCC patients. In vitro and in vivo functional studies revealed that circMALAT1 promoted CSC‐like cells expansion, tumor growth, lung metastasis and drug resistance of ESCC. Mechanistically, circMALAT1 directly interacted with CSC‐functional protein Musashi RNA Binding Protein 2 (MSI2). CircMALAT1 inhibited MSI2 ubiquitination by preventing it from interacting with β‐transducin repeat containing protein (BTRC) E3 ubiquitin ligase. Also, circMALAT1 knockdown inhibited the expression of MSI2‐regulating CSC‐markers c‐Myc in ESCC. Collectively, circMALAT1 modulated the ubiquitination and degradation of the MSI2 protein signaling with ESCC CSCs and accelerated malignant progression of ESCC. CircMALAT1 has the potential to serve as a biomarker for drug resistance and as a target for therapy in CSCs within ESCC. [ABSTRACT FROM AUTHOR]

Published
2024
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38. Novel exosomal circEGFR facilitates triple negative breast cancer autophagy via promoting TFEB nuclear trafficking and modulating miR-224-5p/ATG13/ULK1 feedback loop

Author

Song, Huachen, Zhao, Zitong, Ma, Liying, Zhao, Weihong, Hu, Yi, and Song, Yongmei

Abstract

Triple-negative breast cancer (TNBC) cells are in a more hypoxic and starved state than non-TNBC cells, which makes TNBC cells always maintain high autophagy levels. Emerging evidence has demonstrated that circular RNAs (circRNAs) are involved in the progress of tumorigenesis. However, the regulation and functions of autophagy-induced circRNAs in TNBC remain unclear. In our study, autophagy-responsive circRNA candidates in TNBC cells under amino acid starved were identified by RNA sequencing. The results showed that circEGFR expression was significantly upregulated in autophagic cells. Knockdown of circEGFR inhibited autophagy in TNBC cells, and circEGFR derived from exosomes induced autophagy in recipient cells in the tumor microenvironment. In vitro and in vivo functional assays identified circEGFR as an oncogenic circRNA in TNBC. Clinically, circEGFR was significantly upregulated in TNBC and was positively associated with lymph node metastasis. CircEGFR in plasma-derived exosomes was upregulated in breast cancer patients compared with healthy people. Mechanistically, circEGFR facilitated the translocation of Annexin A2 (ANXA2) toward the plasma membrane in TNBC cells, which led to the release of Transcription Factor EB (a transcription factor of autophagy-related proteins, TFEB) from ANXA2-TFEB complex, causing nuclear translocation of TFEB, thereby promoting autophagy in TNBC cells. Meanwhile, circEGFR acted as ceRNA by directly binding to miR-224-5p and inhibited the expression of miR-224-5p, which weakened the suppressive role of miR-224-5p/ATG13/ULK1 axis on autophagy. Overall, our study demonstrates the key role of circEGFR in autophagy, malignant progression, and metastasis of TNBC. These indicate circEGFR is a potential diagnosis biomarker and therapeutic target for TNBC.

Published
2024
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41. Data from Long Noncoding RNA VESTAR Regulates Lymphangiogenesis and Lymph Node Metastasis of Esophageal Squamous Cell Carcinoma by Enhancing VEGFC mRNA Stability

Author

Wang, Yali, primary, Zhang, Weimin, primary, Liu, Wenzhong, primary, Huang, Lijie, primary, Wang, Yan, primary, Li, Dan, primary, Wang, Guangchao, primary, Zhao, Zitong, primary, Chi, Xinming, primary, Xue, Yu, primary, Song, Yongmei, primary, Liu, Xuefeng, primary, and Zhan, Qimin, primary

Published
2023
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46. Supplementary Data from Long Noncoding RNA VESTAR Regulates Lymphangiogenesis and Lymph Node Metastasis of Esophageal Squamous Cell Carcinoma by Enhancing VEGFC mRNA Stability

Author

Wang, Yali, primary, Zhang, Weimin, primary, Liu, Wenzhong, primary, Huang, Lijie, primary, Wang, Yan, primary, Li, Dan, primary, Wang, Guangchao, primary, Zhao, Zitong, primary, Chi, Xinming, primary, Xue, Yu, primary, Song, Yongmei, primary, Liu, Xuefeng, primary, and Zhan, Qimin, primary

Published
2023
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47. Supplementary Table 4 from DNA Methylation-Mediated Repression of miR-886-3p Predicts Poor Outcome of Human Small Cell Lung Cancer

Author

Cao, Jianzhong, primary, Song, Yongmei, primary, Bi, Nan, primary, Shen, Jie, primary, Liu, Wenyang, primary, Fan, Jing, primary, Sun, Guogui, primary, Tong, Tong, primary, He, Jie, primary, Shi, Yuankai, primary, Zhang, Xun, primary, Lu, Ning, primary, He, Yinghua, primary, Zhang, Hongyu, primary, Ma, Kelong, primary, Luo, Xiaoying, primary, Lv, Lei, primary, Deng, Hui, primary, Cheng, Jing, primary, Zhu, Jingde, primary, Wang, Luhua, primary, and Zhan, Qimin, primary

Published
2023
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48. Data from DNA Methylation-Mediated Repression of miR-886-3p Predicts Poor Outcome of Human Small Cell Lung Cancer

Author

Cao, Jianzhong, primary, Song, Yongmei, primary, Bi, Nan, primary, Shen, Jie, primary, Liu, Wenyang, primary, Fan, Jing, primary, Sun, Guogui, primary, Tong, Tong, primary, He, Jie, primary, Shi, Yuankai, primary, Zhang, Xun, primary, Lu, Ning, primary, He, Yinghua, primary, Zhang, Hongyu, primary, Ma, Kelong, primary, Luo, Xiaoying, primary, Lv, Lei, primary, Deng, Hui, primary, Cheng, Jing, primary, Zhu, Jingde, primary, Wang, Luhua, primary, and Zhan, Qimin, primary

Published
2023
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49. Supplementary Figure 4 from DNA Methylation-Mediated Repression of miR-886-3p Predicts Poor Outcome of Human Small Cell Lung Cancer

Author

Cao, Jianzhong, primary, Song, Yongmei, primary, Bi, Nan, primary, Shen, Jie, primary, Liu, Wenyang, primary, Fan, Jing, primary, Sun, Guogui, primary, Tong, Tong, primary, He, Jie, primary, Shi, Yuankai, primary, Zhang, Xun, primary, Lu, Ning, primary, He, Yinghua, primary, Zhang, Hongyu, primary, Ma, Kelong, primary, Luo, Xiaoying, primary, Lv, Lei, primary, Deng, Hui, primary, Cheng, Jing, primary, Zhu, Jingde, primary, Wang, Luhua, primary, and Zhan, Qimin, primary

Published
2023
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50. Supplementary Table 1 from DNA Methylation-Mediated Repression of miR-886-3p Predicts Poor Outcome of Human Small Cell Lung Cancer

Author

Cao, Jianzhong, primary, Song, Yongmei, primary, Bi, Nan, primary, Shen, Jie, primary, Liu, Wenyang, primary, Fan, Jing, primary, Sun, Guogui, primary, Tong, Tong, primary, He, Jie, primary, Shi, Yuankai, primary, Zhang, Xun, primary, Lu, Ning, primary, He, Yinghua, primary, Zhang, Hongyu, primary, Ma, Kelong, primary, Luo, Xiaoying, primary, Lv, Lei, primary, Deng, Hui, primary, Cheng, Jing, primary, Zhu, Jingde, primary, Wang, Luhua, primary, and Zhan, Qimin, primary

Published
2023
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