C‐MET–dependent signal transduction mediates retinoblastoma growth by regulating PKM2 nuclear translocation

Dai, Hanjun; Zeng, Wen; Luo, Hong

doi:10.1002/cbf.3464

Cited by 6 publications

(8 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The seminal study underscored the pivotal role of nuclear PKM2 in anaerobic glycolysis and tumorigenesis. Subsequently, in another separate study (Dai et al, 2020), the authors completely reproduced the key findings that ERK1/2 phosphorylation promoted the nuclear translocation of PKM2. However, there was also an indication (Zhao, Yuan, et al, 2022) that nuclear PKM2 was independent of phosphorylated ERK1/ 2.…”

Section: Nuclear Pkm2 Cameoed As Transcription Factormentioning

confidence: 74%

“…Generally, nuclear PKM2 acts as a transcription factor that complexes or interacts with histone H3 (Dai et al, 2020), HIF-1α (Wang et al, 2014) or NF-κB p65 (Gu et al, 2021) to enhance the transcription of genes engaging in glycolysis. A direct consequence is that glycolysis was naturally and markedly boosted with PKM2 translocating into the nucleus (Wu, Wang, Zeng, et al, 2022).…”

Section: Nuclear Pkm2 Cameoed As Transcription Factormentioning

confidence: 99%

See 1 more Smart Citation

Positioning determines function: Wandering PKM2 performs different roles in tumor cells

He,

Liang,

Tan

et al. 2023

Cell Biology International

View full text Add to dashboard Cite

Short for pyruvate kinase M2 subtype, PKM2 can be said of all‐round player that is notoriously known for its metabolic involvement in glycolysis. Holding a dural role as a metabolic or non‐metabolic (kinase) enzyme, PKM2 has drawn extensive attention over its biological roles implicated in tumor cells, including proliferation, migration, invasion, metabolism, and so on. wandering PKM2 can be transboundary both intracellularly and extracellularly. Specifically, PKM2 can be nuclear, cytoplasmic, mitochondrial, exosomal, or even circulate within the body. Importantly, PKM2 can function as an RNA‐binding protein (RBP) to self‐support its metabolic function. Despite extensive investigations or reviews available surrounding the biological roles of PKM2 from different angles in tumor cells, little has been described regarding some novel role of PKM2 that has been recently found, including, for example, acting as RNA‐binding protein, protection of Golgi apparatus, and remodeling of microenvironment, and so forth. Given these findings, in this review, we summarize the recent advancements made in PKM2 research, mainly from non‐metabolic respects. By the way, PKM1, another paralog of PKM2, seems to have been overlooked or under‐investigated since its discovery. Some recent discoveries made about PKM1 are also preliminarily mentioned and discussed.

show abstract

Section: Nuclear Pkm2 Cameoed As Transcription Factormentioning

confidence: 74%

Section: Nuclear Pkm2 Cameoed As Transcription Factormentioning

confidence: 99%

Positioning determines function: Wandering PKM2 performs different roles in tumor cells

He,

Liang,

Tan

et al. 2023

Cell Biology International

View full text Add to dashboard Cite

show abstract

“…These results were consistent with its anti-tumor behaviors in other cancers 9,[12][13][14] . Like any other type of cancer cell, RB cells 7,18) were characterized by the uncontrolled growth and increased migration and invasion ability of the tumor cells, the above observations suggested that sinomenine can inhibit the growth and metathesis of WERI-RB-1 and Y79 cells in vitro, suggesting that sinomenine can exert anti-tumor effects in RB.…”

Section: Effect Of Sinomenine Treatment On the Migration As Well As Imentioning

confidence: 80%

Sinomenine Can Inhibit the Growth and Invasion Ability of Retinoblastoma Cell through Regulating PI3K/AKT Signaling Pathway

Zheng

Zhu

et al. 2020

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Sinomenine was found to play anti-cancer functions in different type of cancers, while the mechanisms underlying the anticancer effects of sinomenine in retinoblastoma (RB) remains unclear. The present study was designed to explore the impacts of sinomenine on cell proliferation and invasion ability of RB cells and the related mechanism. Human retinoblastoma cell line WERI-RB-1 and Y79 cells were cultured and treated by different concentration of sinomenine, and then the proliferation ability of the cells was determined via performing the MTT proliferation assay. The cell apoptosis was examined via performing the flow cytometry assay. Then scratch wound healing analysis as well as and transwell invasion analysis have been performed to determine the effect of sinomenine on cell migration ability as well as invasion ability. The proteins level of PI3K/AKT signaling molecules were determined with western blot assay. We found that sinomenine was able to decrease the proliferation and promote the apoptosis of RB cells in a dose-dependent manner; moreover, sinomenine also significantly suppressed the migration as well as invasion ability of WERI-RB-1 and Y79 cells in vitro. Furthermore, sinomenine also deactivated PI3k/AKT signaling in WERI-RB-1 cells via inhibited the phosphorylation of PI3K and AKT proteins. Sinomenine can exert anti-tumor function on RB cells in vitro, therefore sinomenine might be a potential alterative medication for the treatment for RB.

show abstract

“…Therein, PKM2 collaborates with histone H3, thereby stimulating tumor cell growth and facilitating C-MET-dependent synthesis of cyclin D1 and c-Myc. 178 Furthermore, PKM2 modulates the G1/S phase transition by orchestrating the expression of cyclin D1 and effecting phosphorylation of the Bub3 constituent of the spindle assembly checkpoint complex (SAC). Intriguingly, Jiang et al reported that glioblastoma prognosis correlates with the phosphorylation levels of Bub3 at the Y207 residue.…”

Section: Pyruvate Kinasementioning

confidence: 99%

Potential therapies targeting nuclear metabolic regulation in cancer

Chen,

Xu,

Liu

et al. 2023

MedComm

View full text Add to dashboard Cite

The interplay between genetic alterations and metabolic dysregulation is increasingly recognized as a pivotal axis in cancer pathogenesis. Both elements are mutually reinforcing, thereby expediting the ontogeny and progression of malignant neoplasms. Intriguingly, recent findings have highlighted the translocation of metabolites and metabolic enzymes from the cytoplasm into the nuclear compartment, where they appear to be intimately associated with tumor cell proliferation. Despite these advancements, significant gaps persist in our understanding of their specific roles within the nuclear milieu, their modulatory effects on gene transcription and cellular proliferation, and the intricacies of their coordination with the genomic landscape. In this comprehensive review, we endeavor to elucidate the regulatory landscape of metabolic signaling within the nuclear domain, namely nuclear metabolic signaling involving metabolites and metabolic enzymes. We explore the roles and molecular mechanisms through which metabolic flux and enzymatic activity impact critical nuclear processes, including epigenetic modulation, DNA damage repair, and gene expression regulation. In conclusion, we underscore the paramount significance of nuclear metabolic signaling in cancer biology and enumerate potential therapeutic targets, associated pharmacological interventions, and implications for clinical applications. Importantly, these emergent findings not only augment our conceptual understanding of tumoral metabolism but also herald the potential for innovative therapeutic paradigms targeting the metabolism–genome transcriptional axis.

show abstract

C‐MET–dependent signal transduction mediates retinoblastoma growth by regulating PKM2 nuclear translocation

Cited by 6 publications

References 22 publications

Positioning determines function: Wandering PKM2 performs different roles in tumor cells

Positioning determines function: Wandering PKM2 performs different roles in tumor cells

Sinomenine Can Inhibit the Growth and Invasion Ability of Retinoblastoma Cell through Regulating PI3K/AKT Signaling Pathway

Potential therapies targeting nuclear metabolic regulation in cancer

Contact Info

Product

Resources

About