What question did this study set out to answer?

The research aimed to explore BOC's potential as a biomarker for lymphovascular invasion and response to chemotherapy in upper tract urothelial carcinoma.

February 21, 2026Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics0 citations

Pre-Treatment BOC Expression as an Indicator of Lymphovascular Invasion and In Vitro Chemotherapeutic Response in Upper Tract Urothelial Carcinoma

YCYin-Lun Chang HLHao-Lun LuoChang Gung University JPJei-Ming Peng

Key Points

The research aimed to explore BOC's potential as a biomarker for lymphovascular invasion and response to chemotherapy in upper tract urothelial carcinoma.
Sequenced RNA from treatment-naïve stage III UTUC samples to identify BOC expression.
Validated findings in independent cohorts of 74 patients.
Conducted functional assays on cancer cell lines to assess BOC knockdown effects.
Performed methylation-specific PCR to identify regulatory sites for BOC expression.
Used immunohistochemistry to compare BOC levels in high- and low-grade bladder cancer.
Higher BOC expression was significantly associated with lymphovascular invasion (LVI+, p < 0.01).
BOC knockdown significantly reduced cancer cell migration but did not affect cell proliferation.
Knockdown of BOC improved the response to cisplatin and gemcitabine in UTUC cells.
Methylation analysis pinpointed key sites regulating BOC expression.
Increased BOC levels were confirmed in high-grade bladder cancer, correlating with tumor aggressiveness.

Abstract

Background: Upper tract urothelial carcinoma (UTUC) is an aggressive malignancy with high recurrence rates. Lymphovascular invasion (LVI) predicts a poor prognosis, yet its molecular drivers remain unclear. BOC cell adhesion-associated, oncogene-regulated (BOC, also known as Brother of CDO Cell adhesion molecule-Related/Down-regulated by Oncogenes), a hedgehog-related cell surface receptor, may serve as a biomarker for tumor progression and chemotherapy response. The study aimed to investigate the role of BOC in UTUC and its potential to predict LVI and chemotherapy response. Methods: Sequencing (RNA-seq) of 10 stage III UTUC, treatment-naïve, fresh tissue samples identified BOC as a candidate biomarker, which was subsequently validated in 2 independent cohorts (n = 74). Functional assays using urothelial carcinoma cell lines assessed the impact of BOC knockdown on cell migration, proliferation, and drug sensitivity. Methylation-specific PCR (MSP) was used to identify potential regulatory sites influencing BOC expression, and immunohistochemistry (IHC) analysis was conducted to compare BOC levels in high- and low-grade bladder cancer. Results: BOC expression was significantly higher in patients with lymphovascular invasion (LVI+, p < 0.01). Knockdown of BOC markedly inhibited cancer cell migration, without affecting proliferation. BOC knockdown enhanced the efficacy of cisplatin and gemcitabine in UTUC cells, although clinical tissue data did not provide direct evidence of its role as a predictor of drug response. Methylation analysis identified key regulatory sites that may control BOC expression, and IHC confirmed increased BOC levels in high-grade bladder cancer, linking it to tumor aggressiveness. Conclusion: BOC may serve as a potential biomarker for predicting LVI and chemotherapy response in UTUC. Its involvement in cancer cell migration and association with high-grade tumors suggests its clinical relevance for prognosis and treatment stratification. Further validation in larger, multi-center studies is warranted.

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