Chaperone-mediated Autophagy Regulates Cell Growth by Targeting SMAD3 in Glioma

Liu, Hanqun; Yong, Yuxuan; Li, Xingjian; Ye, Panghai; Tao, Kai; Peng, Gongyong; Mo, Mingshu; Guo, Wenyuan; Chen, Xiang; Luo, Yangfu; Lin, Yuwan; Qiu, Jingjun; Zhang, Zhiling; Ding, Liuyan; Zhou, Miaomiao; Yang, Xiuhong; Lin, Li Jen; Yang, Qian; Xu, Pingyi

doi:10.1007/s12264-022-00818-9

Cited by 5 publications

(4 citation statements)

References 51 publications

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“…In addition, another example is the SMAD3 protein, a member of the SMAD (mothers against decapentaplegic) family that acts as an intracellular signal transducer and transcriptional factor induced by TGF-β (transforming growth factor-beta). Likewise, SMAD3 downregulation by CMA augmented proliferation and invasion of glioma cells, supporting the negative correlation between SMAD3 expression and tumor development reported in previous studies ( Liu et al, 2022 ).…”

Section: What Cma Regulatessupporting

confidence: 89%

The role of chaperone-mediated autophagy in drug resistance

Teixeira,

Ramalho,

Souza

et al. 2024

Genet. Mol. Biol.

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In the search for alternatives to overcome the challenge imposed by drug resistance development in cancer treatment, the modulation of autophagy has emerged as a promising alternative that has achieved good results in clinical trials. Nevertheless, most of these studies have overlooked a novel and selective type of autophagy: chaperone-mediated autophagy (CMA). Following its discovery, research into CMA’s contribution to tumor progression has accelerated rapidly. Therefore, we now understand that stress conditions are the primary signal responsible for modulating CMA in cancer cells. In turn, the degradation of proteins by CMA can offer important advantages for tumorigenesis, since tumor suppressor proteins are CMA targets. Such mutual interaction between the tumor microenvironment and CMA also plays a crucial part in establishing therapy resistance, making this discussion the focus of the present review. Thus, we highlight how suppression of LAMP2A can enhance the sensitivity of cancer cells to several drugs, just as downregulation of CMA activity can lead to resistance in certain cases. Given this panorama, it is important to identify selective modulators of CMA to enhance the therapeutic response.

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Section: What Cma Regulatessupporting

confidence: 89%

The role of chaperone-mediated autophagy in drug resistance

Teixeira,

Ramalho,

Souza

et al. 2024

Genet. Mol. Biol.

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“…In contrast, knockdown of LAMP2A expression improved therapeutic properties and sensitivity to cisplatin treatment in mice (Ichikawa et al 2020). In addition, it has been reported that upregulated LAMP2A-mediated hyperactivation of CMA in human grade IV glioblastoma regulates malignant progression of tumor cells by targeting SMAD3 degradation (Liu et al 2022). Upregulation of LAMP2A expression also regulates apoptosis and proliferation of CRC cells (Peng et al 2020).…”

Section: Discussionmentioning

confidence: 99%

LAMP2A regulates cisplatin resistance in colorectal cancer through mediating autophagy

Shi,

Yang,

Shen

et al. 2024

Preprint

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Background Drug resistance is an important constraint on clinical outcomes in advanced cancers. LAMP2A is a limiting protein in molecular chaperone-mediated autophagy. This study was aimed to explore LAMP2A function in cisplatin resistance colorectal cancer (CRC) to seek new ideas for CRC clinical treatment. Methods In this study, LAMP2A expression was analyzed by molecular experimental techniques, such as qRT-PCR and western blot. Then, LAMP2A in cells was interfered by cell transfection experiments. Subsequently, the function of LAMP2A on proliferation, migration, invasion, DDP sensitivity, and autophagy of CRC/DDP cells were further investigated by a series of experiments, such as CCK-8, transwell, and western blot. Results We revealed that LAMP2A was clearly augmented in DDP-resistant CRC and was releated to poor patient prognosis. Functionally, LAMP2A insertion remarkably CRC/DDP proliferation, migration, invasion ability and DDP resistance by strengthen autophagy. In contrast, LAMP2A knockdown limited the proliferation, migration, and invasion while heightened cellular sensitivity to DDP by restraining autophagy in CRC/DDP cells. Furthermore, LAMP2A silencing was able to curb tumor formation and enhance sensitivity to DDP in vivo. Conclusion In summary, LAMP2A boosted malignant progression and DDP resistance in CRC/DDP cells through mediating autophagy. Clarifying LAMP2A function in DDP resistance is promising to seek cancer therapies biomarkers targeting LAMP2A activity.

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“…In contrast, knockdown of LAMP2A expression improved therapeutic properties and sensitivity to DDP treatment in mice (Ichikawa et al 2020 ). In addition, it has been reported that upregulated LAMP2A-mediated hyperactivation of CMA in human grade IV glioblastoma regulates malignant progression of tumor cells by targeting SMAD3 degradation (Liu et al 2022 ). Upregulation of LAMP2A expression also regulates apoptosis and proliferation of CRC cells (Peng et al 2020 ).…”

Section: Discussionmentioning

confidence: 99%

LAMP2A regulates cisplatin resistance in colorectal cancer through mediating autophagy

Shi,

Yang,

Shen

et al. 2024

J Cancer Res Clin Oncol

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Background Drug resistance is an important constraint on clinical outcomes in advanced cancers. LAMP2A is a limiting protein in molecular chaperone-mediated autophagy. This study was aimed to explore LAMP2A function in cisplatin (cis-diamminedichloroplatinum, DDP) resistance colorectal cancer (CRC) to seek new ideas for CRC clinical treatment. Methods In this study, LAMP2A expression was analyzed by molecular experimental techniques,such as qRT-PCR and western blot. Then, LAMP2A in cells was interfered by cell transfection experiments. Subsequently, the function of LAMP2A on proliferation, migration, invasion, DDP sensitivity, and autophagy of CRC/DDP cells were further investigated by a series of experiments, such as CCK-8, transwell, and western blot. Results We revealed that LAMP2A was clearly augmented in DDP-resistant CRC and was related to poor patient prognosis. Functionally, LAMP2A insertion remarkably CRC/DDP proliferation, migration, invasion ability and DDP resistance by strengthen autophagy. In contrast, LAMP2A knockdown limited the proliferation, migration, and invasion while heightened cellular sensitivity to DDP by restraining autophagy in CRC/DDP cells. Furthermore, LAMP2A silencing was able to curb tumor formation and enhance sensitivity to DDP in vivo. Conclusion In summary, LAMP2A boosted malignant progression and DDP resistance in CRC/DDP cells through mediating autophagy. Clarifying LAMP2A function in DDP resistance is promising to seek cancer therapies biomarkers targeting LAMP2A activity.

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Chaperone-mediated Autophagy Regulates Cell Growth by Targeting SMAD3 in Glioma

Cited by 5 publications

References 51 publications

The role of chaperone-mediated autophagy in drug resistance

The role of chaperone-mediated autophagy in drug resistance

LAMP2A regulates cisplatin resistance in colorectal cancer through mediating autophagy

LAMP2A regulates cisplatin resistance in colorectal cancer through mediating autophagy

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