Prevention and Treatment of Side Effects of Immunotherapy for Bladder Cancer

Lou, Kecheng; Feng, Shangzhi; Zhang, Guoxi; Zou, Junrong; Zou, Xiaofeng

doi:10.3389/fonc.2022.879391

Cited by 10 publications

(6 citation statements)

References 117 publications

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“…In addition, immune checkpoint inhibitors, BCG, and platelet-rich plasma are often used for immunotherapy [ 8 – 10 ]. Although neoadjuvant therapy has brought new options for BC treatment, side effects such as inflammation and organ function abnormalities still occur clinically [ 11 ]. Therefore, further exploration of the developmental mechanisms and therapeutic targets associated with BC is essential for the clinical management of BC patients.…”

Section: Introductionmentioning

confidence: 99%

Overexpressed KCNK1 regulates potassium channels affecting molecular mechanisms and biological pathways in bladder cancer

Zhang,

Chen,

Wei

et al. 2024

Eur J Med Res

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Background This study aimed to explore the expression, molecular mechanism and its biological function of potassium two pore domain channel subfamily K member 1 (KCNK1) in bladder cancer (BC). Methods We integrated large numbers of external samples (n = 1486) to assess KCNK1 mRNA expression levels and collected in-house samples (n = 245) for immunohistochemistry (IHC) experiments to validate at the KCNK1 protein level. Single-cell RNA sequencing (scRNA-seq) analysis was performed to further assess KCNK1 expression and cellular communication. The transcriptional regulatory mechanisms of KCNK1 expression were explored by ChIP-seq, ATAC-seq and ChIA-PET data. Highly expressed co-expressed genes (HECEGs) of KCNK1 were used to explore potential signalling pathways. Furthermore, the immunoassay, clinical significance and molecular docking of KCNK1 were calculated. Results KCNK1 mRNA was significantly overexpressed in BC (SMD = 0.58, 95% CI [0.05; 1.11]), validated at the protein level (p < 0.0001). Upregulated KCNK1 mRNA exhibited highly distinguishing ability between BC and control samples (AUC = 0.82 [0.78–0.85]). Further, scRNA-seq analysis revealed that KCNK1 expression was predominantly clustered in BC epithelial cells and tended to increase with cellular differentiation. BC epithelial cells were involved in cellular communication mainly through the MK signalling pathway. Secondly, the KCNK1 transcription start site (TSS) showed promoter-enhancer interactions in three-dimensional space, while being transcriptionally regulated by GRHL2 and FOXA1. Most of the KCNK1 HECEGs were enriched in cell cycle–related signalling pathways. KCNK1 was mainly involved in cellular metabolism–related pathways and regulated cell membrane potassium channel activity. KCNK1 expression was associated with the level of infiltration of various immune cells. Immunotherapy and chemotherapy (docetaxel, paclitaxel and vinblastine) were more effective in BC patients in the high KCNK1 expression group. KCNK1 expression correlated with age, pathology grade and pathologic_M in BC patients. Conclusions KCNK1 was significantly overexpressed in BC. A complex and sophisticated three-dimensional spatial transcriptional regulatory network existed in the KCNK1 TSS and promoted the upregulated of KCNK1 expression. The high expression of KCNK1 might be involved in the cell cycle, cellular metabolism, and tumour microenvironment through the regulation of potassium channels, and ultimately contributed to the deterioration of BC.

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Section: Introductionmentioning

confidence: 99%

Overexpressed KCNK1 regulates potassium channels affecting molecular mechanisms and biological pathways in bladder cancer

Zhang,

Chen,

Wei

et al. 2024

Eur J Med Res

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“…The utilization of immunotherapy to treat cancer has become increasingly popular 163 . Initiating an immunological response toward malignancy in a targeted manner, immunotherapy can be used as a curative anti‐cancer treatment 164 . Immunotherapy targets cancer cells, but it also has the potential to trigger an immune response against healthy cells at any moment during or after treatment.…”

Section: Using Nanomedicine For Bladder Cancer Therapymentioning

confidence: 99%

“…Hence, clinicians and researchers must work toward eliminating or at least mitigating immunotherapy's negative consequences. Activating thioredoxin, transplanting bacterial colonies, and causing iron sagging are only a few of the current immunotherapy innovations and side‐effect mitigation strategies presented by researchers 164 . For immunotherapy to succeed, researchers must find ways to lessen the likelihood of unwanted effects.…”

Section: Using Nanomedicine For Bladder Cancer Therapymentioning

confidence: 99%

“…163 Initiating an immunological response toward malignancy in a targeted manner, immunotherapy can be used as a curative anti-cancer treatment. 164 Immunotherapy targets cancer cells, but it also has the potential to trigger an immune response against healthy cells at any moment during or after treatment. Hence, clinicians and researchers must work toward eliminating or at least mitigating immunotherapy's negative consequences.…”

Section: Using Nanomedicine For Bladder Cancer Therapymentioning

confidence: 99%

“…Activating thioredoxin, transplanting bacterial colonies, and causing iron sagging are only a few of the current immunotherapy innovations and side-effect mitigation strategies presented by researchers. 164 For immunotherapy to succeed, researchers must find ways to lessen the likelihood of unwanted effects. Fortunately, nanocarriers have recently evolved to rise to the occasion.…”

Section: Using Nanomedicine For Bladder Cancer Therapymentioning

confidence: 99%

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miRNAs involvement in the etiology and targeted therapy of bladder cancer: Interaction between signaling pathway

Sharma,

Malviya

2023

Precision Medical Sciences

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Bladder cancer (BC) accounts for roughly 3% of all cancer diagnoses in developed countries. The prognosis could be improved significantly if the cancer is detected and classified as either muscle‐invasive bladder cancer (MIBC) or non‐muscle‐invasive bladder cancer (NMIBC) as promptly as possible. A potential ray of hope for the treatment of BC has emerged with the rapid development of nanomedicine and microRNAs (miRNAs), which promise to have fewer adverse effects, more tumor‐inhibitory effects, and decreased drug resistance. The complex interplay between hereditary and environmental variables is the root cause of this malignancy. Gene expression can be regulated by miRNAs, which are small, non‐coding RNAs that can either prevent the translation of protein‐coding genes or cleave RNA transcripts at certain locations. Elevated genomics has enabled a more extensive investigation of miRNAs whose expression is considerably different in BC patients compared to healthy volunteers or between BC tumor tissues and peripheral tissues. miRNAs have recently been discovered to be important regulators of BC cell carcinogenicity. Inaccurate diagnoses and prolonged treatment delays are more likely to occur due to the current diagnostic process such as lack of sensitivity and specificity and poor image quality. Patients now have access to a plethora of treatment options, including but not limited to surgery, chemotherapy, immunotherapy, gene therapy, and other innovative medicines, and in some cases, combination therapies. BC is one of the deadliest and most disabling malignancies affecting the urinary tract. Cancer of the urinary bladder has a terrible propensity for being fatal. BC is an intricate illness whose development can be affected by multiple parameters. Standard treatments for BC increase prognosis and survival, although recurrence is a major concern for patients. miRNAs are naturally occurring, small RNA molecules that have been linked to cancer through their expression being dysregulated. miRNAs modulate many cellular activities including proliferation, migration, differentiation, and apoptosis. MiRNA dysregulation is recognized in BC, and miRNAs are used as diagnostic and prognostic indicators. However, this manuscript discusses the recent progress made in nanomedicine and the function of miRNAs in the pathogenesis and targeted therapy of BC.

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