Small biomarkers with massive impacts: PI3K/AKT/mTOR signalling and microRNA crosstalk regulate nasopharyngeal carcinoma

Li, Hailong; Deng, Nian-Hua; He, Xiu‐Sheng; Li, Yuehua

doi:10.1186/s40364-022-00397-x

Cited by 16 publications

(12 citation statements)

References 155 publications

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“…Additionally, applying more cutting-edge experimental techniques for verification could enhance the study's quality and comprehensiveness. Furthermore, it is worth noting that some reports suggest miRNA's potential role in regulating PI3K/AKT/mTOR and HIF-α in other tumors [ 45 – 47 ]. Therefore, our future research will explore the mechanism of celastrol in treating B16-F10 melanoma at the molecular level of miRNAs.…”

Section: Discussionmentioning

confidence: 99%

Celastrol inhibits mouse B16-F10 melanoma cell survival by regulating the PI3K/AKT/mTOR signaling pathway and repressing HIF-1α expression

Zhao,

He,

Chen

et al. 2024

Discov Onc

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Objective Melanoma, with its high degree of malignancy, stands as one of the most dangerous skin cancers and remains the primary cause of death from skin cancer. With studies demonstrating the potential of traditional Chinese medicine to intervene and treat melanoma, we turned our attention to celastrol. Celastrol is a triterpene compound extracted from the traditional Chinese medicine derived from Tripterygium wilfordii. Previous studies have shown that celastrol exerts inhibitory effects on various malignant tumors, including melanoma. Hence, our goal was to clarify the impact of celastrol on cell viability, apoptosis, and cell cycle progression by elucidating its effects on the PI3K/AKT/mTOR pathway. Methods CCK-8 and wound healing assays were used to determine the effect of celastrol on the viability and migration of B16-F10 cells. Changes in cell apoptosis, cell cycle, reactive oxygen species (ROS), and mitochondrial membrane potential were detected by flow cytometry. PI3K/AKT/mTOR pathway proteins and HIF-α mRNA expression in B16-F10 cells were detected by western blotting and qPCR. Moreover, the addition of a PI3K activator demonstrated that celastrol could inhibit the function of B16-F10 cells via the PI3K/AKT/mTOR pathway. Results Celastrol inhibited the viability and migration of B16-F10 cells. Through the inhibition of the PI3K/AKT/mTOR pathway down-regulates the expression of HIF-α mRNA, thereby causing an increase of ROS in cells and a decrease in the mitochondrial membrane potential to promote cell apoptosis and cell cycle arrest. The inhibitory effect of celastrol on B16-F10 cells was further demonstrated by co-culturing with a PI3K activator. Conclusion Celastrol inhibits the function of B16-F10 cells by inhibiting the PI3K/AKT/mTOR cellular pathway and regulating the expression of downstream HIF-α mRNA.

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Section: Discussionmentioning

confidence: 99%

Celastrol inhibits mouse B16-F10 melanoma cell survival by regulating the PI3K/AKT/mTOR signaling pathway and repressing HIF-1α expression

Zhao,

He,

Chen

et al. 2024

Discov Onc

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“…In laryngeal squamous cell carcinoma, activation of the PI3K/Akt-NF-κB pathway upregulates MMP2/3 expression, enhancing cell proliferation and migration [ 42 ]. Similarly, the PI3K/AKT pathway has been implicated in the migration and invasion of NPC cells [ 43 ]. For instance, FOXD3 has been found to inhibit cell proliferation, migration, and invasion in NPC by regulating the PI3K-Akt pathway [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Kinesin superfamily member 15 knockdown inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma

Cai,

Lai,

Zhang

et al. 2023

Korean J Physiol Pharmacol

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The aim of this study was to investigate the role of kinesin superfamily member 15 (KIF15) in nasopharyngeal carcinogenesis (NPC) and explore its underlying mechanisms. We employed various assays, including the CCK-8 assay, flow cytometry, the Transwell and scratch assay, Western blotting, and nude mice transplantation tumor, to investigate the impact of KIF15 on NPC. Our findings demonstrate that KIF15 plays a critical role in the proliferation, apoptosis, migration, and invasion of NPC cells. Furthermore, we discovered that silencing KIF15 inhibits cell proliferation, migration, and invasion while promoting apoptosis, and that KIF15's effect on NPC cell growth is mediated through the PI3K/AKT and P53 signaling pathways. Additionally, we showed that KIF15 promotes nasopharyngeal cancer cell growth in vivo . Our study sheds light on the significance of KIF15 in NPC by revealing that KIF15 knockdown inhibits NPC cell growth through the regulation of AKT-related signaling pathways. These findings suggest that KIF15 represents a promising therapeutic target for the prevention and treatment of NPC.

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“… 302 , 342 The PI3K-AKT-mTOR pathway exerts significant impacts on multiple cancers including lung cancer, 344 , 345 ovarian cancer, 302 breast cancer, 346 and NPC. 347 , 348 The PI3K-AKT-mTOR has been proven to be crucial in ovarian tumorigenesis and drug resistance. 302 The level of pAKT is a diagnostic biomarker for the treatment of SCLC involving the combination of clinically approved inhibitors against isoform-specific PI3K and mTOR.…”

Section: Classification Of Tumor Biomarkersmentioning

confidence: 99%

Tumor biomarkers for diagnosis, prognosis and targeted therapy

Zhou,

Tao,

Qiu

et al. 2024

Sig Transduct Target Ther

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Tumor biomarkers, the substances which are produced by tumors or the body’s responses to tumors during tumorigenesis and progression, have been demonstrated to possess critical and encouraging value in screening and early diagnosis, prognosis prediction, recurrence detection, and therapeutic efficacy monitoring of cancers. Over the past decades, continuous progress has been made in exploring and discovering novel, sensitive, specific, and accurate tumor biomarkers, which has significantly promoted personalized medicine and improved the outcomes of cancer patients, especially advances in molecular biology technologies developed for the detection of tumor biomarkers. Herein, we summarize the discovery and development of tumor biomarkers, including the history of tumor biomarkers, the conventional and innovative technologies used for biomarker discovery and detection, the classification of tumor biomarkers based on tissue origins, and the application of tumor biomarkers in clinical cancer management. In particular, we highlight the recent advancements in biomarker-based anticancer-targeted therapies which are emerging as breakthroughs and promising cancer therapeutic strategies. We also discuss limitations and challenges that need to be addressed and provide insights and perspectives to turn challenges into opportunities in this field. Collectively, the discovery and application of multiple tumor biomarkers emphasized in this review may provide guidance on improved precision medicine, broaden horizons in future research directions, and expedite the clinical classification of cancer patients according to their molecular biomarkers rather than organs of origin.

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Small biomarkers with massive impacts: PI3K/AKT/mTOR signalling and microRNA crosstalk regulate nasopharyngeal carcinoma

Cited by 16 publications

References 155 publications

Celastrol inhibits mouse B16-F10 melanoma cell survival by regulating the PI3K/AKT/mTOR signaling pathway and repressing HIF-1α expression

Celastrol inhibits mouse B16-F10 melanoma cell survival by regulating the PI3K/AKT/mTOR signaling pathway and repressing HIF-1α expression

Kinesin superfamily member 15 knockdown inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma

Tumor biomarkers for diagnosis, prognosis and targeted therapy

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