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iNature The overall response to cisplatin-based chemotherapy in bladder urothelial carcinoma (BUC) remains unsatisfactory due to complex pathological subtypes, genomic differences, and drug resistance
.
The genes associated with cisplatin resistance remain unclear
.
On February 7, 2022, Conghui Han of Xuzhou Medical University and Zhesheng Chen of St.
John's University jointly published a research paper titled "Targeting HNRNPU to overcome cisplatin resistance in bladder cancer" in Molecular Cancer (IF=27) online.
A significant correlation was found between HNRNPU expression levels and sensitivity to cisplatin in cancer cell lines
.
In T24 cancer cells overexpressing HNRNPU, knockdown of HNRNPU inhibited cell proliferation, invasion and migration
.
Furthermore, deletion of HNRNPU promoted apoptosis and S-phase arrest in T24 cells treated with cisplatin
.
Data from The Cancer Genome Atlas (TCGA) indicated that HNRNPU was significantly higher in tumor tissues than in normal tissues
.
High HNRNPU levels were negatively correlated with patient survival
.
Transcriptome analysis showed that knockdown of HNRNPU enhanced cisplatin sensitivity by regulating DNA damage repair genes
.
Furthermore, HNRNPU was found to regulate chemosensitivity by affecting the expression of neurofibrin 1 (NF1)
.
In conclusion, this study demonstrates that HNRNPU expression is associated with cisplatin sensitivity in bladder urothelial carcinoma cells
.
Inhibition of HNRNPU may be a potential therapy for cisplatin-resistant bladder cancer
.
Bladder urothelial carcinoma (BUC) is the ninth most common cancer with high mortality worldwide
.
Timely surgery or radiotherapy has become the standard of care for patients with locally non-muscle-invasive BUC
.
However, these treatments are often insufficient to treat recurrent or distant metastatic disease, especially for muscle-invasive BUCs that often develop micrometastases
.
Therefore, systemic chemotherapy has been used simultaneously to control BUC and relieve symptoms
.
Cisplatin-based chemotherapy is the first-line treatment for most cancers, including bladder, breast, and colorectal cancers
.
Although this treatment ideally reduces the risk of death from bladder cancer, the overall response rate in the clinical setting is less than 50%
.
It has been suggested that complex histological subtypes, genomic effects, and acquired cisplatin resistance may reduce its efficiency, thus leaving much room for improving therapeutic response
.
Overexpression of CD147 and monocarboxylate transporter 1 may impair cisplatin sensitivity in bladder cancer
.
Other groups have noted that silencing pyruvate kinase M2 in vitro can overcome cisplatin resistance
.
Unfortunately, the molecules associated with the efficacy of cisplatin remain unclear
.
Therefore, it is necessary to further identify the underlying mechanisms of cisplatin resistance
.
Genome-wide analysis using the CRISPR-Cas9 system is an emerging, efficient and flexible new tool ideal for studying gene function
.
CRISPR libraries have been reported to target thousands of genes and enable negative or positive screening in vivo and in vitro
.
Therefore, it can be used to assess specific relationships between genomic variation and drug response
.
To understand the rationale for cisplatin sensitivity in BUC, the study used a CRISPR screen to investigate genes associated with cisplatin response in T24 cells
.
The results suggest that HNRNPU inhibition impairs tolerance to cisplatin treatment by promoting cisplatin-mediated cell cycle arrest and apoptosis and reducing cell migration
.
Furthermore, this study found that deletion of HNRNPU regulates the interphase chromosomal structure of multiple genes, which may be involved in drug response in BUC
.
In conclusion, this study demonstrates that HNRNPU expression is associated with cisplatin sensitivity in bladder urothelial carcinoma cells
.
Inhibition of HNRNPU may be a potential therapy for cisplatin-resistant bladder cancer
.
Reference message: https://molecular-cancer.
biomedcentral.
com/articles/10.
1186/s12943-022-01517-9
.
The genes associated with cisplatin resistance remain unclear
.
On February 7, 2022, Conghui Han of Xuzhou Medical University and Zhesheng Chen of St.
John's University jointly published a research paper titled "Targeting HNRNPU to overcome cisplatin resistance in bladder cancer" in Molecular Cancer (IF=27) online.
A significant correlation was found between HNRNPU expression levels and sensitivity to cisplatin in cancer cell lines
.
In T24 cancer cells overexpressing HNRNPU, knockdown of HNRNPU inhibited cell proliferation, invasion and migration
.
Furthermore, deletion of HNRNPU promoted apoptosis and S-phase arrest in T24 cells treated with cisplatin
.
Data from The Cancer Genome Atlas (TCGA) indicated that HNRNPU was significantly higher in tumor tissues than in normal tissues
.
High HNRNPU levels were negatively correlated with patient survival
.
Transcriptome analysis showed that knockdown of HNRNPU enhanced cisplatin sensitivity by regulating DNA damage repair genes
.
Furthermore, HNRNPU was found to regulate chemosensitivity by affecting the expression of neurofibrin 1 (NF1)
.
In conclusion, this study demonstrates that HNRNPU expression is associated with cisplatin sensitivity in bladder urothelial carcinoma cells
.
Inhibition of HNRNPU may be a potential therapy for cisplatin-resistant bladder cancer
.
Bladder urothelial carcinoma (BUC) is the ninth most common cancer with high mortality worldwide
.
Timely surgery or radiotherapy has become the standard of care for patients with locally non-muscle-invasive BUC
.
However, these treatments are often insufficient to treat recurrent or distant metastatic disease, especially for muscle-invasive BUCs that often develop micrometastases
.
Therefore, systemic chemotherapy has been used simultaneously to control BUC and relieve symptoms
.
Cisplatin-based chemotherapy is the first-line treatment for most cancers, including bladder, breast, and colorectal cancers
.
Although this treatment ideally reduces the risk of death from bladder cancer, the overall response rate in the clinical setting is less than 50%
.
It has been suggested that complex histological subtypes, genomic effects, and acquired cisplatin resistance may reduce its efficiency, thus leaving much room for improving therapeutic response
.
Overexpression of CD147 and monocarboxylate transporter 1 may impair cisplatin sensitivity in bladder cancer
.
Other groups have noted that silencing pyruvate kinase M2 in vitro can overcome cisplatin resistance
.
Unfortunately, the molecules associated with the efficacy of cisplatin remain unclear
.
Therefore, it is necessary to further identify the underlying mechanisms of cisplatin resistance
.
Genome-wide analysis using the CRISPR-Cas9 system is an emerging, efficient and flexible new tool ideal for studying gene function
.
CRISPR libraries have been reported to target thousands of genes and enable negative or positive screening in vivo and in vitro
.
Therefore, it can be used to assess specific relationships between genomic variation and drug response
.
To understand the rationale for cisplatin sensitivity in BUC, the study used a CRISPR screen to investigate genes associated with cisplatin response in T24 cells
.
The results suggest that HNRNPU inhibition impairs tolerance to cisplatin treatment by promoting cisplatin-mediated cell cycle arrest and apoptosis and reducing cell migration
.
Furthermore, this study found that deletion of HNRNPU regulates the interphase chromosomal structure of multiple genes, which may be involved in drug response in BUC
.
In conclusion, this study demonstrates that HNRNPU expression is associated with cisplatin sensitivity in bladder urothelial carcinoma cells
.
Inhibition of HNRNPU may be a potential therapy for cisplatin-resistant bladder cancer
.
Reference message: https://molecular-cancer.
biomedcentral.
com/articles/10.
1186/s12943-022-01517-9
