Shashen-Maidong Decoction inhibited cancer growth under intermittent hypoxia conditions by suppressing oxidative stress and inflammation

Zheng, Yonghua; Yang, Song; Si, Jianchao; Zhao, Yang; Zhao, Ming; Ji, En-Sheng

doi:10.1016/j.jep.2022.115654

Cited by 11 publications

(2 citation statements)

References 46 publications

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“…4f ). Ki67 has become a very important indicator to evaluate the activity of tumor cells 34 , 35 . Next, the expression of HNRNPK and Ki67 were measured by IHC.…”

Section: Resultsmentioning

confidence: 99%

Single-cell RNA binding protein regulatory network analyses reveal oncogenic HNRNPK-MYC signalling pathway in cancer

et al. 2023

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RNA-binding proteins (RBPs) are key players of gene expression and perturbations of RBP-RNA regulatory network have been observed in various cancer types. Here, we propose a computational method, RBPreg, to identify the RBP regulators by integration of single cell RNA-Seq (N = 233,591) and RBP binding data. Pan-cancer analyses suggest that RBP regulators exhibit cancer and cell specificity and perturbations of RBP regulatory network are involved in cancer hallmark-related functions. We prioritize an oncogenic RBP-HNRNPK, which is highly expressed in tumors and associated with poor prognosis of patients. Functional assays performed in cancer cells reveal that HNRNPK promotes cancer cell proliferation, migration, and invasion in vitro and in vivo. Mechanistic investigations further demonstrate that HNRNPK promotes tumorigenesis and progression by directly binding to MYC and perturbed the MYC targets pathway in lung cancer. Our results provide a valuable resource for characterizing RBP regulatory networks in cancer, yielding potential biomarkers for precision medicine.

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“…4f ). Ki67 has become a very important indicator to evaluate the activity of tumor cells 34 , 35 . Next, the expression of HNRNPK and Ki67 were measured by IHC.…”

Section: Resultsmentioning

confidence: 99%

Single-cell RNA binding protein regulatory network analyses reveal oncogenic HNRNPK-MYC signalling pathway in cancer

et al. 2023

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“…An analysis of hypoxia-related genes uncovered a substantial upregulation of HIF-1α, HIF-2α, and VEGF in LUAD samples compared to normal lung tissue [20]. HIFs play pivotal roles in cellular adaptation to hypoxic conditions and have been associated with various aspects of tumor biology, including angiogenesis, metastasis, and resistance to treatment [21].…”

Section: Discussionmentioning

confidence: 99%

Genomic analysis of hypoxia and mitophagy related genes with prognosis and characterization of the immune microenvironment in LUAD

Liu,

Huang,

Han

et al. 2024

J. Cancer

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Background: Lung adenocarcinoma (LUAD) stands as a prominent subtype within the realm of non-small cell lung cancer and constitutes a primary contributor to cancer-related mortality on a global scale. Notably, hypoxia, a prevalent attribute within solid tumor environments, and mitophagy, a selective manifestation of autophagy dedicated to the removal of damaged mitochondria, have risen to prominence as pivotal factors influencing the initiation and advancement of tumorigenesis. Methods: This investigation harnessed publicly accessible genomic datasets encompassing LUAD patients to delineate genes linked to hypoxia and mitophagy, termed hereafter as hypoxia and mitophagy-related genes (HMRGs). Large-scale repositories furnished both gene expression profiles and clinical particulars. The expression profiles of HMRGs were meticulously scrutinized across 1,093 LUAD specimens, leveraging resources such as The Cancer Genome Atlas and Gene Expression Omnibus datasets. A methodical exploration of HMRG patterns within LUAD led to the discernment of two distinct molecular subtypes. Moreover, a discernible correlation emerged between the subtypes and their respective clinical attributes. A risk scoring system was formulated to prognosticate overall survival (OS) and therapeutic responsiveness in LUAD patients. Subsequently, the reliability of this scoring system was authenticated, and a nomogram was adopted to refine the clinical utility range of the risk score. The proliferation and migration impacts of KRT8 on LUAD cells were evaluated through cck8 assays, edu assays, and transwell assays, the results were further validated in vivo. Results: Elevated risk scores were indicative of unfavorable OS probabilities. Furthermore, these risk scores exhibited associations with immune checkpoints and chemotherapeutic drug sensitivity. Collectively, our exhaustive analysis of HMRGs in LUAD patients unveiled their conceivable participation in configuring the multifaceted tumor microenvironment, encompassing clinicopathological attributes and prognosis. A sequence of experiments illuminated the pro-proliferative and pro-migratory attributes of KRT8 in vitro and vivo, thus underscoring its carcinogenic potential. Conclusions: In this study, we have unearthed innovative gene signatures tethered to HMRGs, which harbor prognostic implications concerning patient outcomes. These insights hold potential for steering the development of targeted therapeutic modalities tailored for LUAD.

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The effects of Atractylodes macrocephala extract BZEP self-microemulsion based on gut–liver axis HDL/LPS signaling pathway to ameliorate metabolic dysfunction-associated fatty liver disease in rats

Li,

Jiang,

Dong

et al. 2024

Biomedicine & Pharmacotherapy

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Shashen-Maidong Decoction inhibited cancer growth under intermittent hypoxia conditions by suppressing oxidative stress and inflammation

Cited by 11 publications

References 46 publications

Single-cell RNA binding protein regulatory network analyses reveal oncogenic HNRNPK-MYC signalling pathway in cancer

Single-cell RNA binding protein regulatory network analyses reveal oncogenic HNRNPK-MYC signalling pathway in cancer

Genomic analysis of hypoxia and mitophagy related genes with prognosis and characterization of the immune microenvironment in LUAD

The effects of Atractylodes macrocephala extract BZEP self-microemulsion based on gut–liver axis HDL/LPS signaling pathway to ameliorate metabolic dysfunction-associated fatty liver disease in rats

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