Characterization and function of biomarkers in sunitinib-resistant renal carcinoma cells

Wang, Yali; Liu, Hui; Wan, Lilin; Pan, Ke-Hao; Ni, Jia-Xuan; Hu, Qiang; Xu, Bin

doi:10.1016/j.gene.2022.146514

Cited by 5 publications

(3 citation statements)

References 35 publications

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“…Highly expressed RIGI and MX2 lead to an increase in the level of certain immune checkpoints that act as inhibitors of immune surveillance and allow tumours to grow. MX2 might encourage VEGF synthesis by activating the Janus kinase (JAK)–STAT pathway, leading to drug resistance to sunitinib (Wang et al, 2022). These two genes could be potential biomarkers for sunitinib‐resistant renal cell carcinoma.…”

Section: Present and Potential Biomarkers Of Sunitinib Resistancementioning

confidence: 99%

“…MX2 might encourage VEGF synthesis by T A B L E 1 Summary of targets and strategies to overcome sunitinib resistance in renal cell carcinoma (RCC). activating the Janus kinase (JAK)-STAT pathway, leading to drug resistance to sunitinib (Wang et al, 2022). These two genes could be potential biomarkers for sunitinib-resistant renal cell carcinoma.…”

Section: Present and Potential Biomarkers Of Sunitinib Resistancementioning

confidence: 99%

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Mechanisms of sunitinib resistance in renal cell carcinoma and associated opportunities for therapeutics

Wang,

Liu,

Gong

et al. 2023

British J Pharmacology

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Sunitinib is the first‐line drug for renal cell carcinoma (RCC) treatment. However, patients who received sunitinib treatment will ultimately develop drug resistance after 6‐15 months, creating a huge obstacle to the current treatment of RCC. Therefore, it is urgent to clarify the mechanisms of sunitinib resistance and develop new strategies to overcome it. In this review, the mechanisms of sunitinib resistance in RCC have been summarized based on five topics: activation of bypass or alternative pathway, inadequate drug accumulation, tumor microenvironment, metabolic reprogramming and epigenetic regulation. Furthermore, present and potential biomarkers, as well as potential treatment strategies for overcoming sunitinib resistance in RCC are illustrated.

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Section: Present and Potential Biomarkers Of Sunitinib Resistancementioning

confidence: 99%

Section: Present and Potential Biomarkers Of Sunitinib Resistancementioning

confidence: 99%

Mechanisms of sunitinib resistance in renal cell carcinoma and associated opportunities for therapeutics

Wang,

Liu,

Gong

et al. 2023

British J Pharmacology

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“…In addition, 25% of the KIRC patients are diagnosed with metastasis at the first visit due to no specific features at the early stage [ 10 , 11 ]. As for metastatic renal cell carcinoma, only few first-line drugs such as Sunitinib can be used, but drug resistance often occurs after 6-15 months of systematic treatment [ 12 ]. Identifying key driver genes related to progression can help improve the prognosis.…”

Section: Introductionmentioning

confidence: 99%

Identification of molecular characteristics of FUT8 and alteration of core fucosylation in kidney renal clear cell cancer

Xin,

Wen,

Zhou

et al. 2024

Aging

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Background: Kidney renal clear cell cancer (KIRC) is a type of urological cancer that occurs worldwide. Core fucosylation (CF), as the most common post-translational modification, is involved in the tumorigenesis. Methods: The alterations of CF-related genes were summarized in pan-cancer. The “ConsensusClusterPlus” package was utilized to identify two CF-related KIRC subtypes. The “ssgsea” function was chosen to estimate the CF score, signaling pathways and cell deaths. Multiple algorithms were applied to assess immune responses. The “oncoPredict” was utilized to estimate the drug sensitivity. The IHC and subgroup analysis was performed to reveal the molecular features of FUT8. Single-cell RNA sequencing (scRNA-seq) data were scrutinized to evaluate the CF state. Results: In pan-cancer, there was a noticeable alteration in the expression of CF-related genes. In KIRC, two CF-related subtypes (i.e., C1, C2) were obtained. In comparison to C2, C1 exhibited a higher CF score and correlated with poorer overall survival. Additionally, the TME of C2 demonstrated increased activity in neutrophils, macrophages, myeloid dendritic cells, and B cells, alongside a higher presence of silent mast cells, NK cells, and endothelial cells. Compared to normal samples, higher expression of FUT8 is observed in KIRC. The mutation of SETD2 was more frequent in low-FUT8 samples while the mutation of DNAH9 was more frequent in high-FUT8 samples. scRNA-seq analyses revealed that the CF score was predominantly higher in endothelial cells and fibroblast cells. Conclusions: Two CF-related subtypes with distinct prognosis and TME were identified in KIRC. FUT8 exhibited elevated expression in KIRC samples.

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Investigations on the electrochemical behavior of sunitinib and metabolites N-desethyl-sunitinib and sunitinib-N-oxide and its selective determination using molecularly imprinted polymer-based sensor

Budak,

Cetinkaya,

Kaya

et al. 2023

Electrochimica Acta

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Characterization and function of biomarkers in sunitinib-resistant renal carcinoma cells

Cited by 5 publications

References 35 publications

Mechanisms of sunitinib resistance in renal cell carcinoma and associated opportunities for therapeutics

Mechanisms of sunitinib resistance in renal cell carcinoma and associated opportunities for therapeutics

Identification of molecular characteristics of FUT8 and alteration of core fucosylation in kidney renal clear cell cancer

Investigations on the electrochemical behavior of sunitinib and metabolites N-desethyl-sunitinib and sunitinib-N-oxide and its selective determination using molecularly imprinted polymer-based sensor

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