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Resistance to the chemotherapeutic drug cisplatin has been documented in various types of cancer, while the increased expression of β-catenin has been observed in cisplatin-resistant ovarian cancer. However, the involvement of β-catenin in cisplatin resistance is unclear. The present study investigated the antitumor effect of cisplatin on the proliferation, invasion and apoptosis of breast cancer (Bc) cells following β-catenin silencing in Bc, which is the most frequent type of malignancy among women. The expression of β-catenin in Bc tissues and cell lines was measured by reverse transcription-quantitative polymerase chain reaction, and the association between expression levels and clinical characteristics was statistically analyzed. The viability of Bc cell lines treated with siR-β-catenin or with siR-β-catenin and cisplatin in combination was determined using a cell counting Kit-8 assay. The migratory and invasive abilities of Bc cells treated with both siR-β-catenin and cisplatin were examined with Transwell assays. The cd44 antigen/intercellular adhesion molecule 1 expression ratio, cell cycle distribution and apoptosis levels of Bc cells treated with siR-β-catenin and cisplatin in combination were detected by flow cytometry. The expression levels of apoptosis-associated proteins, including caspase-3/9, in the Bc cells treated with both siR-β-catenin and cisplatin were investigated by western blot analysis. The levels of apoptosis in the Bc cells following combined treatment with siR-β-catenin and cisplatin was further quantified by Hoechst 33342 staining. β-catenin was identified to be highly expressed in Bc tissues and cell lines and was associated with pathological stage and lymph node status. Following knockdown of β-catenin expression, cisplatin treatment suppressed the viabilities, and the migratory and invasive capabilities of the T47d and McF-7 cells, and induced extensive apoptosis. β-catenin knockdown upregulated caspase-3/9 levels following cisplatin treatment and induced the apoptosis of T47d and McF-7 cells. In conclusion, β-catenin may be of value as a therapeutic target during cisplatin treatment in patients with Bc treated with cisplatin.

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Clustered regularly interspaced short palindromic repeats (CRISPR)-Cas12a, which exhibits excellent target DNA-activated trans-cleavage activity under the guidance of a programmable CRISPR RNA (crRNA), has shown great promise in next-generation biosensing technology. However, current CRISPR-Cas12a-based biosensors usually improve sensitivity by the initial nucleic acid amplification, while the distinct programmability and predictability of the crRNA-guided target binding process has not been fully exploited. Herein, we, for the first time, propose a modular and sensitive CRISPR-Cas12a fluorometric aptasensor by integrating an enzyme-free and robust crRNA-mediated catalytic nucleic acid network, namely, Cas12a-CMCAN, in which crRNA acts as an initiator to actuate cascade toehold-mediated strand displacement reactions (TM-SDRs). As a proof of concept, adenosine triphosphate (ATP) was selected as a model target. Owing to the multiturnover of CRISPR-Cas12a trans-cleavage and the inherent recycling amplification network, this method achieved a limit of detection value of 0.16 μM (20-fold lower than direct Cas12a-based ATP detection) with a linear range from 0.30 to 175 μM. In addition, Cas12a-CMCAN can be successfully employed to detect ATP levels in diluted human serum samples. Considering the simplicity, sensitivity, and easy to tune many targets by changing aptamer sequences, the Cas12a-CMCAN sensing method is expected to offer a heuristic idea for the development of CRISPR-Cas12a-based biosensors and unlock its potential for general and convenient molecule diagnostics.