The Obscure Potential of AHNAK2

Zardab, Mohamed; Stasinos, Konstantinos; Grose, Richard; Kocher, Hemant M.

doi:10.3390/cancers14030528

Cited by 19 publications

(14 citation statements)

References 84 publications

(167 reference statements)

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“…3 Additionally, AHNAK2, shown to promote UM cell proliferation and migration, 9 was found to correlate with infiltration of immune cell subpopulations such as CD8 + and CD4 + . 10 Our findings align with a recent report by Figueiredo et al, 5 which revealed that the downregulation of TLR1, a gene responsible for immune activation, is correlated with M3 status but not BAP1 expression, indicating epigenomic reprogramming independent of BAP1 mutations. These results highlight the importance of further exploring epigenetic regulation of the unique immune landscape of UM, which presents both challenges and opportunities for developing effective treatments for high-risk patients.…”

supporting

confidence: 92%

Uncovering accurate prognostic markers for high‐risk uveal melanoma through DNA methylation profiling

Šoltýsová

Dvorska

Kajabova

et al. 2023

Clinical & Translational Med

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supporting

confidence: 92%

Uncovering accurate prognostic markers for high‐risk uveal melanoma through DNA methylation profiling

Šoltýsová

Dvorska

Kajabova

et al. 2023

Clinical & Translational Med

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“…AHNAK nucleoprotein 2 (AHNAK2) is a member of the AHNAK protein family with a molecular weight greater than 600 kDa, 8 , 9 and its function has been gradually unveiled in recent years. Studies have reported that AHNAK2 is closely associated with oncogenesis in clear cell renal carcinoma, 10 thyroid carcinoma, 11 lung adenocarcinoma, 12 and uveal melanoma.…”

Section: Introductionmentioning

confidence: 99%

AHNAK2 Promotes the Progression of Pancreatic Ductal Adenocarcinoma by Maintaining the Stability of c-MET

Chen,

Miao,

Lin

et al. 2024

CMAR

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Purpose Pancreatic ductal adenocarcinoma (PDAC) is extremely malignant and rapidly progresses. The overall response rate of PDAC to current treatment methods is still unsatisfactory. Thus, identifying novel targets and clarifying the underlying mechanisms associated with PDAC progression may potentially offer additional treatment strategies. AHNAK2 is aberrantly expressed in a variety of tumors and exerts pro-tumorigenic effects. However, the biological role of AHNAK2 in PDAC remains poorly understood. Methods The expression of AHNAK2 in PDAC and paired non-tumor tissues was detected by immunohistochemistry (IHC) and quantitative real-time polymerase chain reaction (qRT-PCR). Lentivirus knockdown was performed to investigate the impact of AHNAK2 on the biological function of pancreatic cancer cells. The subcutaneous cell-derived xenograft (CDX) model and the KPC spontaneous mouse model with AHNAK2 silencing were used to observe the effects of AHNAK2 on tumor growth and prognosis. The expression of c-MET at protein level in response to HGF treatment was assessed using western blot. Results Our results demonstrated that AHNAK2 was highly expressed in PDAC clinical samples and associated with poor prognosis. Knockdown of AHNAK2 significantly inhibited the proliferation, migration, and invasion of pancreatic cancer cells. AHNAK2 knockdown or knockout resulted in tumor growth suppression and prolonged survival in mice with PDAC. In addition, AHNAK2 and c-MET expression levels showed a significant positive correlation at the post-transcriptional level. Mechanistically, AHNAK2 promoted tumor progression by preventing c-MET degradation and persistently activating the HGF/c-MET signaling pathway. Conclusion Overall, our study revealed that AHNAK2 plays an important role in PDAC progression by modulating the c-MET signaling pathway, and targeting AHNAK2 may be an effective therapeutic strategy for PDAC.

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“…In addition, a bioinformatic analysis indicated that AHNAK2 expression was positively correlated with CD4 + T cells, macrophages and neutrophils, although there was no careful experimental data or any rigorous hypothesis testing to back it up 15 . The latest review of AHNAKs has been delivered by Zardab et al, and provides a detailed summary of protein structure and oncology functions 16 …”

Section: Introductionmentioning

confidence: 99%

“…15 The latest review of AHNAKs has been delivered by Zardab et al, and provides a detailed summary of protein structure and oncology functions. 16 In this investigation, we detected the AHNAK2 expression levels in tumor and paired normal tissues and explored cancer databases from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) for gene expression and survival analysis. To verify our results from databases and explore the role of AHNAK2 in LUAD, we performed tumor cell phenotype assays, gene enrichment analysis and coimmunoprecipitation tests.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of AHNAK2 inhibits cell cycle of lung adenocarcinoma cells by interacting with RUVBL1

Shao

Miao

et al. 2023

Thoracic Cancer

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Background Lung adenocarcinoma (LUAD) is the leading cause of death among cancer diseases. The tumorigenic functions of AHNAK2 in LUAD have attracted more attention in recent years, while there are few studies which have reported its high molecular weight. Methods The mRNA‐seq data of AHNAK2 and corresponding clinical data from UCSC Xena and GEO was analyzed. LUAD cell lines were transfected with sh‐NC and sh‐AHNAK2, and cell proliferation, migration and invasion were then detected by in vitro experiments. We performed RNA sequencing and mass spectrometry analysis to explore the downstream mechanism and interacting proteins of AHNAK2. Finally, western blot, cell cycle analysis and CO‐IP were used to confirm our assumptions regarding previous experiments. Results Our study revealed that AHNAK2 expression was significantly higher in tumors than in normal lung tissues and higher AHNAK2 expression led to a poor prognosis, especially in patients with advanced tumors. AHNAK2 suppression via shRNA reduced the LUAD cell lines proliferation, migration and invasion and induced significant changes in DNA replication, NF‐kappa B signaling pathway and cell cycle. AHNAK2 knockdown also caused G1/S phase cell cycle arrest, which could be attributed to the interaction of AHNAK2 and RUVBL1. In addition, the results from gene set enrichment analysis (GSEA) and RNA sequencing suggested that AHNAK2 probably plays a part in the mitotic cell cycle. Conclusion AHNAK2 promotes proliferation, migration and invasion in LUAD and regulates the cell cycle via the interaction with RUVBL1. More studies of AHNAK2 are still needed to reveal its upstream mechanism.

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The Obscure Potential of AHNAK2

Cited by 19 publications

References 84 publications

Uncovering accurate prognostic markers for high‐risk uveal melanoma through DNA methylation profiling

Uncovering accurate prognostic markers for high‐risk uveal melanoma through DNA methylation profiling

AHNAK2 Promotes the Progression of Pancreatic Ductal Adenocarcinoma by Maintaining the Stability of c-MET

Downregulation of AHNAK2 inhibits cell cycle of lung adenocarcinoma cells by interacting with RUVBL1

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