Machine learning-driven SERS analysis platform for rapid and accurate detection of precancerous lesions of gastric cancer.

A novel approach is proposed leveraging surface-enhanced Raman spectroscopy (SERS) combined with machine learning (ML) techniques, principal component analysis (PCA)-centroid displacement-based nearest neighbor (CDNN). This label-free approach can identify slight abnormalities between SERS spectra of gastric lesions at different stages, offering a promising avenue for detection and prevention of precancerous lesion of gastric cancer (PLGC). The agaric-shaped nanoarray substrate was prepared using gas-liquid interface self-assembly and reactive ion etching (RIE) technology to measure SERS spectra of serum from mice model with gastric lesions at different stages, and then a SERS spectral recognition model was trained and constructed using the PCA-CDNN algorithm. The results showed that the agaric-shaped nanoarray substrate has good uniformity, stability, cleanliness, and SERS enhancement effect. The trained PCA-CDNN model not only found the most important features of PLGC, but also achieved satisfactory classification results with accuracy, area under curve (AUC), sensitivity, and specificity up to 100%. This demonstrated the enormous potential of this analysis platform in the diagnosis of PLGC.

Surface-enhanced Raman scatting microfluidic chip based on the identification competition strategy were used for rapid and simultaneous detection of liver cancer related proteins.

Biomarker testing plays a crucial role in the early detection of liver cancer. Herein, we developed a dual-signal amplification approach utilizing magnetic aggregation and a recognition competition strategy for the simultaneous detection of alpha-fetoprotein (AFP) and manganese superoxide dismutase (MnSOD) in serum. 4-MBA@AuNPs@H1 and DTNB@AuNPs@H2 were synthesized by functionalizing Raman signaling molecules and aptamer complementary chains onto the surface of gold nanoparticles (AuNPs). The detection complex Raman signal molecule@AuNPs@H-Fe3O4@cDNA was assembled by conjugating 4-MBA@AuNPs@H1 and DTNB@AuNPs@H2 with two nucleic acid aptamers (cDNA1 and cDNA2) modified with Fe3O4 through partial base complementary pairing. The target protein exhibited specific binding with the aptamer, leading to the competitive displacement of 4-MBA@AuNPs@H1 and DTNB@AuNPs@H2 from the Fe3O4 array surface, consequently resulting in a reduction of the Surface-Enhanced Raman Spectroscopy (SERS) signal. Through this approach, the limit of detection (LOD) for AFP and MnSOD in serum was achieved at remarkably low levels of 5.89 pg/mL and 6.23 pg/mL, respectively, with a reaction incubation period of only 5 min. Finally, the platform was utilized for the quantification of AFP and MnSOD in the serum of a nude mouse hepatocellular carcinoma model. The results obtained through SERS were consistent with those from enzyme-linked immunosorbent assay (ELISA), validating its accuracy. This methodology presents a novel approach for the swift and concurrent detection of proteins, holding significant clinical promise for the early diagnosis of hepatocellular carcinoma.

Dowregulation of OTX1 attenuates gastric cancer cell proliferation, migration and invasion.

Orthodenticle homolog 1 (OTX1) has previously been revealed to be tightly associated with the development and progression of several human tumors. However, the functional roles and underlying molecular mechanisms of OTX1 in gastric cancer (GC) remain poorly understood. In the present study, we observed that OTX1 was highly expressed in GC tissues compared with adjacent non­tumor tissues based on a large cohort of samples from The Cancer Genome Atlas (TCGA) database. An immunohistochemical analysis indicated that OTX1 levels were increased in tumors that became metastatic compared with those in tumors that did not. This finding was significantly associated with patients who had shorter overall survival times. The knockdown of OTX1 significantly inhibited the proliferation, migration and invasion of SGC­7901 and MGC­803 cells. Furthermore, the knockdown of OTX1 induced cell cycle arrest in the G0/G1 phase and reduced the expression of cyclin D1. In addition, the inhibition of OTX1 led to increased GC cell apoptosis by upregulating cleaved PARP, cleaved caspase­3 and Bax. In conclusion, our data indicated that OTX1 functions as a key regulator in tumor growth and metastasis of GC cells. Thus, OTX1 may be a promising novel target for molecular therapy directed toward GC.