Research Progress on the Relationship Between Mitochondrial Deoxyguanosine Kinase and Apoptosis and Autophagy in Lung Adenocarcinoma Cells

Liu, Chao; Qin, Qin; Cong, Hongliang

doi:10.58567/ci01010004

Cited by 8 publications

(3 citation statements)

References 29 publications

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“…Lung cancer can be divided into two main types: small-cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) [1][2][3]. NSCLC, which includes adenocarcinoma, squamous cell carcinoma, and large cell carcinoma, is the more common type of lung cancer, accounting for about 80-85% of all cases [4]. SCLC accounts for the remaining 15-20% of cases.…”

Section: Introductionmentioning

confidence: 99%

PRMT5 facilitates angiogenesis and EMT via HIF-1α/VEGFR/Akt signaling axis in lung cancer

Zheng¹,

Ji²,

Yi³

et al. 2023

Aging

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Abnormal angiogenesis is a critical factor in tumor growth and metastasis, and protein arginine methyltransferase 5 (PRMT5), a prominent type II enzyme, is implicated in various human cancers. However, the precise role of PRMT5 in regulating angiogenesis to promote lung cancer cell metastasis and the underlying molecular mechanisms are not fully understood. Here, we show that PRMT5 is overexpressed in lung cancer cells and tissues, and its expression is triggered by hypoxia. Moreover, inhibiting or silencing PRMT5 disrupts the phosphorylation of the VEGFR/Akt/eNOS angiogenic signaling pathway, NOS activity, and NO production. Additionally, inhibiting PRMT5 activity reduces HIF-1α expression and stability, resulting in the down-regulation of the VEGF/VEGFR signaling pathway. Our findings indicate that PRMT5 promotes lung cancer epithelial-mesenchymal transition (EMT), which might be possibly through controlling the HIF-1α/VEGFR/Akt/eNOS signaling axis. Our study provides compelling evidence of the close association between PRMT5 and angiogenesis/EMT and highlights the potential of targeting PRMT5 activity as a promising therapeutic approach for treating lung cancer with abnormal angiogenesis.

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Section: Introductionmentioning

confidence: 99%

PRMT5 facilitates angiogenesis and EMT via HIF-1α/VEGFR/Akt signaling axis in lung cancer

Zheng¹,

Ji²,

Yi³

et al. 2023

Aging

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show abstract

“…Lung cancer is a major global health issue and is responsible for a significant number of cancer‐related deaths, accounting for about 18% of all cancer deaths 1–3 . Smoking is the primary risk factor for lung cancer, but exposure to air pollution, radon gas and occupational hazards can also increase the risk.…”

Section: Introductionmentioning

confidence: 99%

“…

Lung cancer is a major global health issue and is responsible for a significant number of cancer-related deaths, accounting for about 18% of all cancer deaths. [1][2][3] Smoking is the primary risk factor for lung cancer, but exposure to air pollution, radon gas and occupational hazards can also increase the risk. Despite advances in diagnosis and treatment, including improved imaging techniques and targeted therapies, lung cancer remains challenging to treat, particularly in advanced stages.

…”

mentioning

confidence: 99%

PRMT5activatesKLF5by methylation to facilitate lung cancer

Zhou¹,

Chang²,

Zhang³

et al. 2023

J Cellular Molecular Medi

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The highly expressed oncogenic factor Krüppel‐like factor 5 (KLF5) promotes various cancerous processes, such as cell growth, survival, anti‐apoptosis, migration and metastasis, particularly in lung cancer. Nevertheless, the modifications to KLF5 after translation are poorly understood. Protein arginine methyltransferase 5 (PRMT5) is considered as an oncogene known to be involved in different types of carcinomas, including lung cancer. Here, we show that the expression levels of PRMT5 and KLF5 are highly expressed lung cancer. Moreover, PRMT5 interacts with KLF5 and facilitates the dimethylation of KLF5 at Arginine 41 in a manner that depends on methyltransferase activity. Downregulation or pharmaceutical suppression of PRMT5 reduces the expression of KLF5 and its downstream targets both in vitro and in vivo. Mechanistically, the dimethylation of KLF5 by PRMT5 promotes the maintenance and proliferation of lung cancer cells at least partially by stabilising KLF5 via regulation of the Akt/GSK3β signalling axis. In summary, PRMT5 methylates KLF5 to prevent its degradation, thereby promoting the maintenance and proliferation of lung cancer cells. These results suggest that targeting PRMT5/KLF5 axis may offer a potential therapeutic strategy for lung cancer.

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Targeting MAPK14 in microglial cells: neuroimmune implications ofPanax ginsengin post-stroke inflammation

Guan,

Yang,

Yang

et al. 2024

Journal of Pharmacy and Pharmacology

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Aim This study investigates the molecular mechanisms through which Panax ginseng and Panax notoginseng saponin (PNS) mitigate neuroinflammatory damage and promote neural repair postischemic stroke, utilizing bioinformatics, and experimental approaches. Background Cerebral infarction significantly contributes to disability worldwide, with chronic neuroinflammation worsening cognitive impairments and leading to neurodegenerative diseases. Addressing neuroimmune interactions is crucial for slowing disease progression and enhancing patient recovery, highlighting the need for advanced research in neuroimmune regulatory mechanisms and therapeutic strategies. Objective To elucidate the effects of the traditional Chinese medicine components Panax ginseng and PNS on neuroinflammatory damage following ischemic stroke, focusing on the molecular pathways involved in mitigating inflammation and facilitating neural repair. Methods The study employs single-cell sequencing and transcriptomic analysis to investigate gene expression changes associated with cerebral infarction. Gene set enrichment analysis and weighted gene co-expression network analysis are used to identify key molecular markers and core genes. Furthermore, pharmacological profiling, including functional assays, assesses the impact of Ginsenoside-Rc, a PNS derivative, on microglial cell viability, cytokine production, and reactive oxygen species (ROS) levels. Results Our analysis revealed that MAPK14 is a critical mediator in the neuroinflammatory response to ischemic stroke. Ginsenoside-Rc potentially targets and modulates MAPK14 activity to suppress inflammation. Experimental validation showed that Ginsenoside-Rc treatment, combined with MAPK14 silencing, significantly alters MAPK14 expression and mitigates neuroinflammatory damage, evidenced by reduced microglial cell death, inflammatory factor secretion, and ROS production. Conclusion Ginsenoside-Rc’s modulation of MAPK14 offers a promising therapeutic strategy for reducing neuroinflammation and potentially improving cognitive recovery post-ischemic stroke. This supports the therapeutic application of the traditional Chinese medicine Sanqi in ischemic stroke care, providing a theoretical and experimental foundation for its use. Others Future work will focus on extending these findings through clinical trials to evaluate the efficacy and safety of Ginsenoside-Rc in human subjects, aiming to translate these promising preclinical results into practical therapeutic interventions for ischemic stroke recovery.

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Research Progress on the Relationship Between Mitochondrial Deoxyguanosine Kinase and Apoptosis and Autophagy in Lung Adenocarcinoma Cells

Cited by 8 publications

References 29 publications

PRMT5 facilitates angiogenesis and EMT via HIF-1α/VEGFR/Akt signaling axis in lung cancer

PRMT5 facilitates angiogenesis and EMT via HIF-1α/VEGFR/Akt signaling axis in lung cancer

PRMT5activatesKLF5by methylation to facilitate lung cancer

Targeting MAPK14 in microglial cells: neuroimmune implications ofPanax ginsengin post-stroke inflammation

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