Andrographolide suppresses non-small-cell lung cancer progression through induction of autophagy and antitumor immune response

Wang, Xuan-Run; Jiang, Ze‐Bo; Xu, Cong; Meng, Wei-Yu; Liu, Pei; Zhang, Yizhong; Xie, Chun; Xu, Jingyi; Xie, Ya-Jia; Liang, Tu-Liang; Yan, Hao-Xin; Fan, Xing‐Xing; Yao, Xiaojun; Wu, Qibiao; Leung, Elaine Lai‐Han

doi:10.1016/j.phrs.2022.106198

Cited by 28 publications

(13 citation statements)

References 69 publications

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“…Autophagy is an essential intracellular process for cellular quality control, and is usually regarded as a survival strategy in mammalian cells through anti‐inflammatory, 53 anti‐tumor immune response pathway 54 and so on. While the role of autophagy in AS progression seems to be complex.…”

Section: Discussionmentioning

confidence: 99%

N‐acetylneuraminic acid modulates SQSTM1/p62 sialyation‐mediated ubiquitination degradation contributing to vascular endothelium dysfunction in experimental atherosclerosis mice

Chen,

Qiu,

Chen

et al. 2023

IUBMB Life

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Sialic acid (SIA) has been reported to be a risk factor for atherosclerosis (AS) due to its high plasma levels in such patients. However, the effect of increasing SIA in circulation on endothelial function during AS progression remains unclear. In the present study, ApoE−/− mice and endothelial cells line (HUVEC cells) were applied to investigate the effect of SIA on AS progression and its potential molecular mechanism. In vivo, mice were injected intraperitoneally with Neu5Ac (main form of SIA) to keep high‐level SIA in circulation. ORO, H&E, and Masson staining were applied to detect the plaque progression. In vitro, HUVECs were treated with Neu5Ac at different times, CCK‐8, RT‐PCR, western blot, and immunoprecipitation methods were used to analyze its effects on endothelial function and the potential involved mechanism. Results from the present study showed that high plasma levels of Neu5Ac in ApoE−/− mice could aggravate the plaque areas as well as increase necrotic core areas and collagen fiber contents. Remarkably, Neu5Ac levels in circulation displayed a positive correlation with AS plaque areas. Furthermore, results from HUVECs showed that Neu5Ac inhibited cells viability in a time/dose‐dependent manner, by then induced the activation of inflammation makers such as ICAM‐1 and IL‐1β. Mechanism study showed that the activation of excessive autophagy medicated by SQSTM1/p62 displayed an important role in endothelium inflammatory injury. Neu5Ac could modify SQSTM1/p62 as a sialylation protein, and then increase its level with ubiquitin binding, further inducing ubiquitination degradation and being involved in the excessive autophagy pathway. Inhibition of sialylation by P‐3Fax‐Neu5Ac, a sialyltransferase inhibitor, reduced the binding of SQSTM1/p62 to ubiquitin. Together, these findings indicated that Neu5Ac increased SQSTM1/p62‐ubiquitin binding through sialylation modification, thereby inducing excessive autophagy and subsequent endothelial injury. Inhibition of SQSTM1/p62 sialylation might be a potential strategy for preventing such disease with high levels of Neu5Ac in circulation.

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Section: Discussionmentioning

confidence: 99%

N‐acetylneuraminic acid modulates SQSTM1/p62 sialyation‐mediated ubiquitination degradation contributing to vascular endothelium dysfunction in experimental atherosclerosis mice

Chen,

Qiu,

Chen

et al. 2023

IUBMB Life

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“…The role of autophagy in cancer is multifaceted and context dependent. Although some controversy exists, targeting autophagy has been proposed as a potential therapeutic strategy for cancer treatment [ 37 , 38 ]. Rapamycin, an FDA-approved drug known to activate autophagy via mTORC1, has demonstrated antitumor effects across various malignancies.…”

Section: Discussionmentioning

confidence: 99%

YAP1 Regulates the YAP1/AR/PSA Axis through Autophagy in Castration-Resistant Prostate Cancer and Mediates T-Cell Immune and Inflammatory Cytokine Infiltration

Wang,

Wu,

et al. 2024

Biomedicines

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The emergence of castration-resistant prostate cancer (CRPC) following androgen deprivation therapy (ADT) is associated with increased malignancy and limited treatment options. This study aims to investigate potential connections between immune cell infiltration and inflammatory cytokines with the YAP1/AR/PSA axis by exploring their interactions with autophagy. Our research reveals heightened levels of Yes-associated protein 1 (YAP1) expression in CRPC tissues compared with tissues from androgen-dependent prostate cancer (ADPC) and benign prostate hyperplasia (BPH). Additionally, a correlation was observed between YAP1 and PSA expressions in CRPC tissues, suggesting that YAP1 may exert a regulatory influence on PSA expression within CRPC. Enhanced YAP1 expression in C4-2 cells resulted in the upregulation of androgen receptor (AR) nuclear translocation and intracellular prostate-specific antigen (PSA) levels. Conversely, the suppression of YAP1 led to a decrease in PSA expression, suggesting that YAP1 may positively regulate the PSA in castration-resistant prostate cancer (CRPC) by facilitating AR nuclear import. The modulation of the autophagy activity exerts a significant impact on the expression levels of YAP1, the AR, and the PSA. Moreover, recent advancements in immunity and inflammation studies present promising avenues for potential therapies targeting prostate cancer (PC).

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“…This work clarified the particular component by which Andro inhibits NSCLC cell proliferation. Treatment with a combination of Andro and anti‐PD‐1 mAb immunotherapy will likely become a treatment for patients with NSCLC 87 …”

Section: Small‐molecule Compounds Targeting Autophagy For the Treatme...mentioning

confidence: 99%

Targeted therapy for non‐small‐cell lung cancer: New insights into regulated cell death combined with immunotherapy

Li,

Wang,

et al. 2023

Immunological Reviews

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SummaryNon‐small‐cell lung cancer (NSCLC), which has a high rate of metastatic spread and drug resistance, is the most common subtype of lung cancer. Therefore, NSCLC patients have a very poor prognosis and a very low chance of survival. Human cancers are closely linked to regulated cell death (RCD), such as apoptosis, autophagy, ferroptosis, pyroptosis, and necroptosis. Currently, small‐molecule compounds targeting various types of RCD have shown potential as anticancer treatments. Moreover, RCD appears to be a specific part of the antitumor immune response; hence, the combination of RCD and immunotherapy might increase the inhibitory effect of therapy on tumor growth. In this review, we summarize small‐molecule compounds used for the treatment of NSCLC by focusing on RCD and pharmacological systems. In addition, we describe the current research status of an immunotherapy combined with an RCD‐based regimen for NSCLC, providing new ideas for targeting RCD pathways in combination with immunotherapy for patients with NSCLC in the future.

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Andrographolide suppresses non-small-cell lung cancer progression through induction of autophagy and antitumor immune response

Cited by 28 publications

References 69 publications

N‐acetylneuraminic acid modulates SQSTM1/p62 sialyation‐mediated ubiquitination degradation contributing to vascular endothelium dysfunction in experimental atherosclerosis mice

N‐acetylneuraminic acid modulates SQSTM1/p62 sialyation‐mediated ubiquitination degradation contributing to vascular endothelium dysfunction in experimental atherosclerosis mice

YAP1 Regulates the YAP1/AR/PSA Axis through Autophagy in Castration-Resistant Prostate Cancer and Mediates T-Cell Immune and Inflammatory Cytokine Infiltration

Targeted therapy for non‐small‐cell lung cancer: New insights into regulated cell death combined with immunotherapy

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