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学者姓名：王娟
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Abstract ：
Salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, Sal) is a catechol isoquinoline that causes neurotoxicity and shares structural similarity with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, an environmental toxin that causes Parkinson's disease. However, the mechanism by which Sal mediates dopaminergic neuronal death remains unclear. In this study, we found that Sal significantly enhanced the global level of N-6-methyladenosine (m(6)A) RNA methylation in PC12 cells, mainly by inducing the downregulation of the expression of m(6)A demethylases fat mass and obesity-associated protein (FTO) and alkB homolog 5 (ALKBH5). RNA sequencing analysis showed that Sal downregulated the Hippo signaling pathway. The m(6)A reader YTH domain-containing family protein 2 (YTHDF2) promoted the degradation of m(6)A-containing Yes-associated protein 1 (YAP1) mRNA, which is a downstream key effector in the Hippo signaling pathway. Additionally, downregulation of YAP1 promoted autophagy, indicating that the mutual regulation between YAP1 and autophagy can lead to neurotoxicity. These findings reveal the role of Sal on m(6)A RNA methylation and suggest that Sal may act as an RNA methylation inducer mediating dopaminergic neuronal death through YAP1 and autophagy. Our results provide greater insights into the neurotoxic effects of catechol isoquinolines compared with other studies and may be a reference for assessing the involvement of RNA methylation in the pathogenesis of Parkinson's disease.
Keyword ：
YTHDF2 YTHDF2 FTO FTO salsolinol salsolinol RNA methylation RNA methylation YAP1 YAP1 Hippo pathway Hippo pathway autophagy autophagy ALKBH5 ALKBH5 m(6)A m(6)A Parkinson's disease Parkinson's disease
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| GB/T 7714 | Wang, Jianan , Ran, Yuanyuan , Li, Zihan et al. Salsolinol as an RNA m6A methylation inducer mediates dopaminergic neuronal death by regulating YAP1 and autophagy [J]. | NEURAL REGENERATION RESEARCH , 2025 , 20 (3) : 887-899 . |
| MLA | Wang, Jianan et al. "Salsolinol as an RNA m6A methylation inducer mediates dopaminergic neuronal death by regulating YAP1 and autophagy" . | NEURAL REGENERATION RESEARCH 20 . 3 (2025) : 887-899 . |
| APA | Wang, Jianan , Ran, Yuanyuan , Li, Zihan , Zhao, Tianyuan , Zhang, Fangfang , Wang, Juan et al. Salsolinol as an RNA m6A methylation inducer mediates dopaminergic neuronal death by regulating YAP1 and autophagy . | NEURAL REGENERATION RESEARCH , 2025 , 20 (3) , 887-899 . |
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Abstract ：
ATG9A is a transmembrane protein essential for macroautophagy/autophagy that drives autophagosome formation by delivering essential proteins and lipids to the phagophore through vesicle trafficking. Here, we demonstrate that the atypical Rho GTPase RHOD is required for ATG9A trafficking and stimulates autophagosome formation. Upon starvation, RHOD interacted with ATG9A and accompanied ATG9A trafficking from the Golgi toward phagophores. In addition, starvation-induced high levels of RHOD resulted in Golgi fragmentation to further promote ATG9A vesicle export from the trans-Golgi network to the peripheral region. Loss of RHOD suppressed ATG9A trafficking and reduced the distribution of ATG9A on the phagophore. Moreover, WHAMM (WASP homolog associated with actin, golgi membranes and microtubules) forms a complex with RHOD and participates in this process in a RHOD-dependent manner. Importantly, RHOD mutants, which lack the exon II-containing effector region motif that is required for ATG9A binding or lack the CAAX box that is responsible for membrane targeting, fail to stimulate ATG9A trafficking and autophagosome formation. Furthermore, RHOD plays a distinct suppressor role in tumor development, partly associated with its regulatory effect on autophagy. These findings reveal the important roles of RHOD in autophagy and tumor development.Abbreviation: ATG9A: autophagy related 9A; BafA1: bafilomycin A1; BiFC: bimolecular fluorescence complementation; co-IP: co-immunoprecipitation; EBSS: Earle's balanced salt solution; FM: full culture medium; KO: knockout; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; PUP-IT: pupylation-based interaction tagging; RHOD: ras homolog family member D; SQSTM1: sequestosome 1; TGN: trans-Golgi network; VC: Venus C-terminal; VN: Venus N-terminal; WHAMM: WASP homolog associated with actin, golgi membranes and microtubules; WIPI2: WD repeat domain, phosphoinositide interacting 2; WT: wild-type; 3-MA: phosphatidylinositol 3-kinase (PtdIns3K) inhibitor 3-methyladenine.
Keyword ：
vesicle trafficking vesicle trafficking WHAMM WHAMM autophagy autophagy RHOD RHOD ATG9A ATG9A lung cancer lung cancer
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| GB/T 7714 | Wang, Sijia , Ren, Jing , Chi, Jinghan et al. RHOD mediates ATG9A trafficking to promote autophagosome formation during autophagy in cancer [J]. | AUTOPHAGY , 2025 , 21 (9) : 1976-1994 . |
| MLA | Wang, Sijia et al. "RHOD mediates ATG9A trafficking to promote autophagosome formation during autophagy in cancer" . | AUTOPHAGY 21 . 9 (2025) : 1976-1994 . |
| APA | Wang, Sijia , Ren, Jing , Chi, Jinghan , Guan, Yifei , Zheng, Ran , Wang, Juan et al. RHOD mediates ATG9A trafficking to promote autophagosome formation during autophagy in cancer . | AUTOPHAGY , 2025 , 21 (9) , 1976-1994 . |
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Abstract ：
Unconventional protein secretion (UcPS) encompasses diverse non-canonical cellular export mechanisms that operate independently of the classical secretory pathway, representing a crucial cellular response to various physiological and pathological conditions. This comprehensive review synthesizes current understanding of UcPS mechanisms, particularly focusing on their roles in disease pathogenesis and progression. Recent advances in proteomics and cellular biology have revealed that UcPS facilitates the secretion of various biomedically significant proteins, including inflammatory mediators, growth factors, and disease-associated proteins, through multiple pathways such as membrane translocation, secretory lysosomes, and membrane-bound organelles. Notably, dysregulation of UcPS mechanisms has been implicated in various pathological conditions, including chronic inflammation, neurodegenerative disorders, and malignant transformation. We critically evaluate the molecular machinery governing UcPS, its regulation under cellular stress, and its contribution to disease mechanisms. Furthermore, we examine emerging therapeutic strategies targeting UcPS pathways, highlighting both opportunities and challenges in developing novel interventional approaches.
Keyword ：
Inflammation Inflammation Neurodegenerative diseases Neurodegenerative diseases Unconventional protein secretion Unconventional protein secretion Cancer Cancer
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| GB/T 7714 | Liu, Yukun , Zhang, Haolin , Li, Xianghua et al. Molecular mechanisms and pathological implications of unconventional protein secretion in human disease: from cellular stress to therapeutic targeting [J]. | MOLECULAR BIOLOGY REPORTS , 2025 , 52 (1) . |
| MLA | Liu, Yukun et al. "Molecular mechanisms and pathological implications of unconventional protein secretion in human disease: from cellular stress to therapeutic targeting" . | MOLECULAR BIOLOGY REPORTS 52 . 1 (2025) . |
| APA | Liu, Yukun , Zhang, Haolin , Li, Xianghua , He, Tianlong , Zhang, Wenting , Ji, Cuicui et al. Molecular mechanisms and pathological implications of unconventional protein secretion in human disease: from cellular stress to therapeutic targeting . | MOLECULAR BIOLOGY REPORTS , 2025 , 52 (1) . |
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Abstract ：
SNARE is a crucial membrane fusion factor. It forms SNARE complex that play significant roles in regulating various biological functions. The SNARE protein family, including syntaxin13 (STX13), is highly conserved across various species, from yeast to humans. This review summarizes the molecular mechanisms by which STX13-associated SNARE complexes contribute to diverse endosome-mediated membrane fusions. Furthermore, multiple cofactors are essential for regulating the SNARE complexes-mediated membrane fusion. These include but are not limited to Rab GTPases and their effectors. The interaction of these factors with SNARE proteins constitutes a critical component driving vesicle fusion processes.
Keyword ：
Syntaxin13 Syntaxin13 SNARE SNARE Endosome Endosome
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| GB/T 7714 | Zhang, Wenting , Zhang, Haolin , He, Tianlong et al. The diverse functions of syntaxin 13 in endosome-mediated membrane fusion [J]. | INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES , 2025 , 307 . |
| MLA | Zhang, Wenting et al. "The diverse functions of syntaxin 13 in endosome-mediated membrane fusion" . | INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES 307 (2025) . |
| APA | Zhang, Wenting , Zhang, Haolin , He, Tianlong , Li, Xianghua , Liu, Yukun , Han, Huijie et al. The diverse functions of syntaxin 13 in endosome-mediated membrane fusion . | INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES , 2025 , 307 . |
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Abstract ：
Macroautophagy involves the encapsulation of cellular components within double-membrane autophagosomes for subsequent degradation in vacuoles or lysosomes. Coat protein complex II (COPII) vesicles serve as a membrane source for autophagosome formation. However, the specific role of SEC24D, an isoform of the COPII coat protein SEC24, in the macroautophagy pathway remains unclear. In this study, we demonstrate that SEC24D is indispensable for macroautophagy and important for autophagosome closure. Depletion of SEC24D leads to the accumulation of unsealed isolation membranes. Furthermore, under conditions of starvation, SEC24D interacts with casein kinase1 delta (CK1 delta), a member of the casein kinase 1 family, and autophagy-related 9A (ATG9A). Collectively, our findings unveil the indispensable role of SEC24D in starvation-induced autophagy in mammalian cells.
Keyword ：
isolation membrane isolation membrane autophagosome closure autophagosome closure COPII COPII SEC24D SEC24D autophagy autophagy
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| GB/T 7714 | He, Tianlong , Ji, Cuicui , Zhang, Wenting et al. The COPII coat protein SEC24D is required for autophagosome closure in mammals [J]. | FEBS LETTERS , 2024 , 598 (23) : 2897-2909 . |
| MLA | He, Tianlong et al. "The COPII coat protein SEC24D is required for autophagosome closure in mammals" . | FEBS LETTERS 598 . 23 (2024) : 2897-2909 . |
| APA | He, Tianlong , Ji, Cuicui , Zhang, Wenting , Li, Xianghua , Liu, Yukun , Wang, Xiaoli et al. The COPII coat protein SEC24D is required for autophagosome closure in mammals . | FEBS LETTERS , 2024 , 598 (23) , 2897-2909 . |
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Abstract ：
Aloperine is an alkaloid found in the seeds and leaves of the medicinal plant Sophora alopecuroides L. It has been used as herbal medicine in China for centuries due to its potent anti-inflammatory, antioxidant, antibacterial, and antiviral properties. Recently, aloperine has been widely investigated for its therapeutic activities. Aloperine is proven to be an effective therapeutic agent against many human pathological conditions, including cancer, viral diseases, and cardiovascular and inflammatory disorders. Aloperine is reported to exert therapeutic effects through triggering various biological processes, including cell cycle arrest, apoptosis, autophagy, suppressing cell migration, and invasion. It has also been found to be associated with the modulation of various signaling pathways in different diseases. In this review, we summarize the most recent knowledge on the modulatory effects of aloperine on various critical biological processes and signaling mechanisms, including the PI3K, Akt, NF-kappa B, Ras, and Nrf2 pathways. These data demonstrate that aloperine is a promising therapeutic candidate. Being a potent modulator of signaling mechanisms, aloperine can be employed in clinical settings to treat various human disorders in the future.
Keyword ：
autophagy autophagy Ras Ras PI3K/Akt PI3K/Akt cell cycle cell cycle Nrf2 Nrf2 NF-kappa B NF-kappa B apoptosis apoptosis
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| GB/T 7714 | Tahir, Muhammad , Ali, Sakhawat , Zhang, Wenting et al. Aloperine: A Potent Modulator of Crucial Biological Mechanisms in Multiple Diseases [J]. | BIOMEDICINES , 2022 , 10 (4) . |
| MLA | Tahir, Muhammad et al. "Aloperine: A Potent Modulator of Crucial Biological Mechanisms in Multiple Diseases" . | BIOMEDICINES 10 . 4 (2022) . |
| APA | Tahir, Muhammad , Ali, Sakhawat , Zhang, Wenting , Lv, Boqiang , Qiu, Wenge , Wang, Juan . Aloperine: A Potent Modulator of Crucial Biological Mechanisms in Multiple Diseases . | BIOMEDICINES , 2022 , 10 (4) . |
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Abstract ：
To obtain new anticancer agents with antimetastatic adjunct efficacy, a series of novel N-4-hydrazone derivatives of 5,7-dihydro-6H-pyrrolo[2,3-d]pyrimidin-6-one were designed and synthesized by an eight-step reaction, with appropriate yields. All the synthesized compounds were evaluated for their antiproliferative activity against A549 and MCF-7 cells and for antiplatelet aggregation activity in vitro. The results showed that compounds 25 and 35 not only showed potent antiproliferative activity against the A549 (IC50 = 15.3 and 21.4 mu M) and MCF-7 (IC50 = 15.6 and 10.9 mu M) cell lines but also showed certain antiplatelet aggregation activity (inhibition rates: 47.0% and 45.8%). These results indicated that the structural modification on the N-4-hydrazone moiety of 5,7-dihydro-6H-pyrrolo[2,3-d]pyrimidin-6-one is promising to obtain novel anticancer compounds with antimetastatic adjunct efficacy. In addition, a molecular docking study was performed to investigate the possible targets, and these results indicated that compounds 25 and 35 have the potential to target EGFR, HER2, and P2Y(12).
Keyword ：
antimetastatic antimetastatic 3-d]pyrimidin-6-one 3-d]pyrimidin-6-one anticancer anticancer synthesis synthesis hydrazone hydrazone pyrrolo[2 pyrrolo[2
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| GB/T 7714 | Zhao, Zhichang , Wang, Hongjun , Tian, Nana et al. Synthesis and biological evaluation of N-4-hydrazone derivatives of 5,7-dihydro-6H-pyrrolo[2,3-d]pyrimidin-6-one as novel anticancer agents with antimetastatic adjunct efficacy [J]. | ARCHIV DER PHARMAZIE , 2021 , 354 (11) . |
| MLA | Zhao, Zhichang et al. "Synthesis and biological evaluation of N-4-hydrazone derivatives of 5,7-dihydro-6H-pyrrolo[2,3-d]pyrimidin-6-one as novel anticancer agents with antimetastatic adjunct efficacy" . | ARCHIV DER PHARMAZIE 354 . 11 (2021) . |
| APA | Zhao, Zhichang , Wang, Hongjun , Tian, Nana , Yan, Hong , Wang, Juan . Synthesis and biological evaluation of N-4-hydrazone derivatives of 5,7-dihydro-6H-pyrrolo[2,3-d]pyrimidin-6-one as novel anticancer agents with antimetastatic adjunct efficacy . | ARCHIV DER PHARMAZIE , 2021 , 354 (11) . |
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Abstract ：
Autophagy is an evolutionarily conserved pathway, in which cytoplasmic components are sequestered within double-membrane vesicles called autophagosomes and then transported into lysosomes or vacuoles for degradation. Over 40 conserved autophagy-related (ATG) genes define the core machinery for the five processes of autophagy: initiation, nucleation, elongation, closure, and fusion. In this review, we focus on one of the least well-characterized events in autophagy, namely the closure of the isolation membrane/phagophore to form the sealed autophagosome. This process is tightly regulated by ESCRT machinery, ATG proteins, Rab GTPase and Rab-related proteins, SNAREs, sphingomyelin, and calcium. We summarize recent progress in the regulation of autophagosome closure and discuss the key questions remaining to be addressed.
Keyword ：
closure closure isolation membrane isolation membrane autophagosome autophagosome autophagy autophagy
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| GB/T 7714 | Jiang, Wenyan , Chen, Xuechai , Ji, Cuicui et al. Key Regulators of Autophagosome Closure [J]. | CELLS , 2021 , 10 (11) . |
| MLA | Jiang, Wenyan et al. "Key Regulators of Autophagosome Closure" . | CELLS 10 . 11 (2021) . |
| APA | Jiang, Wenyan , Chen, Xuechai , Ji, Cuicui , Zhang, Wenting , Song, Jianing , Li, Jie et al. Key Regulators of Autophagosome Closure . | CELLS , 2021 , 10 (11) . |
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Abstract ：
Autophagy is a conserved degradation process crucial to maintaining the primary function of cellular and organismal metabolism. Impaired autophagy could develop numerous diseases, including cancer, cardiomyopathy, neurodegenerative disorders, and aging. N6-methyladenosine (m6A) is the most common RNA modification in eukaryotic cells, and the fate of m6A modified transcripts is controlled by m6A RNA binding proteins. m6A modification influences mRNA alternative splicing, stability, translation, and subcellular localization. Intriguingly, recent studies show that m6A RNA methylation could alter the expression of essential autophagy-related (ATG) genes and influence the autophagy function. Thus, both m6A modification and autophagy could play a crucial role in the onset and progression of various human diseases. In this review, we summarize the latest studies describing the impact of m6A modification in autophagy regulation and discuss the role of m6A modification-autophagy axis in different human diseases, including obesity, heart disease, azoospermatism or oligospermatism, intervertebral disc degeneration, and cancer. The comprehensive understanding of the m6A modification and autophagy interplay may help in interpreting their impact on human diseases and may aid in devising future therapeutic strategies.
Keyword ：
m6A m6A Azoospermatism Azoospermatism RNA methylation RNA methylation Cancer Cancer Autophagy Autophagy Obesity Obesity Ischemic heart disease Ischemic heart disease
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| GB/T 7714 | Chen, Xuechai , Wang, Jianan , Tahir, Muhammad et al. Current insights into the implications of m6A RNA methylation and autophagy interaction in human diseases [J]. | CELL AND BIOSCIENCE , 2021 , 11 (1) . |
| MLA | Chen, Xuechai et al. "Current insights into the implications of m6A RNA methylation and autophagy interaction in human diseases" . | CELL AND BIOSCIENCE 11 . 1 (2021) . |
| APA | Chen, Xuechai , Wang, Jianan , Tahir, Muhammad , Zhang, Fangfang , Ran, Yuanyuan , Liu, Zongjian et al. Current insights into the implications of m6A RNA methylation and autophagy interaction in human diseases . | CELL AND BIOSCIENCE , 2021 , 11 (1) . |
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Abstract ：
Purpose Non-small cell lung cancer (NSCLC) is the most common type of lung cancer and ranked top in terms of incidence and mortality in men and women. Recently, improvements in treatment approaches for NSCLC have reported, but still, there is a need to devise innovative treatment strategies, especially to manage the advanced and metastatic stage of NSCLC. Aloperine (ALO), an herbal alkaloid, has exerted anti-cancer effects in many cancers. However, the use of any chemotherapeutic agents is dose limited due to possible adverse effects and drug-resistance issues. Therefore, a combination of chemotherapy with viral-based targeted gene therapy may provide a novel treatment strategy for NSCLC. Methods/results In this study, the results of the MTT and flow cytometry-based assays showed that Aloperine-Adbic (adenoviral vector expressing p14(ARF)/p53) combined treatment on NSCLC cells synergistically produced anti-proliferative effects, induced apoptosis, and arrested cell cycle at the G1 phase. Furthermore, the expression analysis suggested that the p53/p21 pathway might contribute to achieving aforesaid cytotoxic effects. The ALO-Adbic combined treatment prolonged the percent survival of NSCLC xenograft models. Conclusion In conclusion, ALO-Adbic combination can produce synergistic anti-cancer effects at low doses, and may offer a more effective and less toxic new treatment strategy for NSCLC.
Keyword ：
NSCLC NSCLC Aloperine Aloperine Adenoviral vectors Adenoviral vectors p53 p53 Synergy Synergy
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| GB/T 7714 | Muhammad, Tahir , Sakhawat, Ali , Khan, Aamir Ali et al. Aloperine in combination with therapeutic adenoviral vector synergistically suppressed the growth of non-small cell lung cancer [J]. | JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY , 2020 , 146 (4) : 861-874 . |
| MLA | Muhammad, Tahir et al. "Aloperine in combination with therapeutic adenoviral vector synergistically suppressed the growth of non-small cell lung cancer" . | JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY 146 . 4 (2020) : 861-874 . |
| APA | Muhammad, Tahir , Sakhawat, Ali , Khan, Aamir Ali , Huang, Hua , Khan, Haroon Rashid , Huang, Yinghui et al. Aloperine in combination with therapeutic adenoviral vector synergistically suppressed the growth of non-small cell lung cancer . | JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY , 2020 , 146 (4) , 861-874 . |
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