[Retracted] lncRNA SNHG3 promotes breast cancer progression by acting as a miR­326 sponge.

Following the publication of the above article, the authors have requested that it be retracted. Subsequently to having performed these experiments, the authors have realized that their MCF­7 cells had become contaminated while performing the colony formation and transwell experiments. Furthermore, they were unable to reproduce the results from the in vivo experiments, and knockdown of SNHG3 was found not to affect tumor growth in nude mice. Following a further investigation in the Editorial Office, it also came to light that there were other possible anomalies associated with the presentation of the tumor images in Fig. 6B and the colony formation assay data in Fig. 2C. Therefore, theos article has been retracted from the Journal; all the authors agree to this retraction. The Editor and the authors would like to apologize for any inconvenience caused. [the original article was published in Oncology Reports 44: 1502­1510, 2020; DOI: 10.3892/or.2020.7690].

lncRNA SNHG3 promotes breast cancer progression by acting as a miR­326 sponge.

Accumulating evidence suggests that long noncoding RNA (lncRNA) small nucleolar RNA host gene 3 (SHNG3) plays crucial roles in the initiation and progression of various types of malignant cancers. Yet, the role played by SNHG3 in breast cancer as well as the associated mechanisms remain largely unclear. The expression of SNHG3 was detected in breast cancer tissues and cell lines by reverse­transcription quantitative PCR (RT­qPCR). Cell proliferation, colony formation, cell cycle distribution, migration and invasion abilities were detected by Cell Counting Kit­8, colony formation assay, flow cytometry, wound­healing and Matrigel invasion assays, respectively. The regulatory relationships between SNHG3 and miR­326 were explored by luciferase reporter assay. A nude mouse model was established to investigate the effect of SNHG3 in vivo. The results showed an upregulation of SNHG3 in breast cancer tissues and cell lines. Loss­of­function assays revealed significant suppression of breast cancer behaviors such as: Abilities to proliferate, form colonies, migrate and invade in vitro coupled with a delayed growth of tumors in vivo when SNHG3 was knocked down. Mechanically, it was shown that SNHG3 served as a competing endogenous RNA (ceRNA) of miR­326 that in turn is a tumor suppressor in this cancer. The correlation between the expression of SNHG3 and miR­326 was found to be strongly negative in these samples. Additionally, we found that inhibition of SNHG3 caused a partially reversal in the inhibition exerted by miR­326 on the ability of these cells to proliferate, form colonies, migrate and invade. Collectively, these findings suggest the functioning of SNHG3 as a ceRNA to enhance the ability of breast cancer cells to proliferate and metastasize to putatively serve as a new target to explore therapeutic intervention of this malignancy.

Characterization and imaging of surgical specimens of invasive breast cancer and normal breast tissues with the application of Raman spectral mapping: A feasibility study and comparison with randomized single-point detection method.

A mapping technique was used in the present study to explore the biological and imaging characteristics of invasive breast cancer and normal breast tissues in Raman examination data and construct a diagnostic model for breast cancer. Raman examination data reflect the biochemical or molecular characteristics of the target tissues. A total of 45 specimens from patients with breast cancer who underwent surgery and 25 adjacent normal breast tissue specimens were included in the present study. Using the specimens, a total of 53 sets of mapping data and 2,597 pieces of Raman spectral data were obtained. The collected spectra were corrected and fitted, the Raman spectra were analyzed by robust statistical methods, and a diagnostic model was constructed using the k-Nearest Neighbor (KNN) method. The KNN classification method was applied to analyze the characteristics of the mapping test application. The percentage of outliers in the mapping data for malignant and normal breast tissues was 12.7 and 6.6%, respectively. The percentage of outlier data in the conventional single-point detection data for malignant and normal breast tissues was 24.5 and 26.0%, respectively. Analysis using a t-test identified a significant difference in the number of outliers between mapping and single-point detection for malignant (t=-6.169; P<0.001) and normal breast tissues (t=-8.873; P<0.001). Based on the mapping data, the accuracy, sensitivity and specificity for breast cancer detection by the diagnostic model constructed using the KNN method was 99.56, 96.6 and 98.48%, respectively. The positive and negative predictive value of this model was 99.56 and 89.04%, respectively. The data obtained by mapping technology demonstrated improved stability and contained less outliers compared with single-point detection. The diagnostic model constructed using the mapping data demonstrated excellent diagnostic performance and good correspondence with pathological results. The findings of the present study demonstrated the feasibility of the application of the diagnostic model for intraoperative real-time imaging for patients with breast cancer. This study provided the foundation of Raman spectroscopy-based diagnostic imaging at the molecular level.

Functional analyses of microRNA-326 in breast cancer development.

MicroRNA-326 (miR-326) was reported to be dysregulated and involved in the progression of multiple cancers. However, the clinical significance, biological role and underlying mechanism of miR-326 in the carcinogenesis of breast cancer are still unclear. In the present study, we showed that miR-326 was down-regulated in human breast cancer tissues and cell lines. Our results also revealed that miR-326 overexpression significantly suppressed breast cancer cell proliferation, migration and invasion, and induced cell cycle arrest at G1/G0 phase. Furthermore, Sex determining region Y-box (SOX) protein 12 (SOX12), a known oncogene, was identified as a direct target of miR-326 by luciferase reporter assay. Moreover, miR-326 expression was inversely correlated with SOX12 mRNA expression levels in human breast cancer specimens. Overexpression of SOX12 partially rescued the inhibitory effect on cell proliferation, migration and invasion in breast cancer cells caused by miR-326 overexpression. These findings suggested that miR-326 might play a suppressive role in breast cancer, at least in part, by targeting SOX12, rendering miR-326 a promising therapeutic target for breast cancer.