Breast cancer is the most common malignancy in women and microRNA-768-3p (miR-768-3p) is abnormally expressed in hepatocellular carcinoma, non-small cell lung carcinomas and melanoma. The aim of the present study was to evaluate the prognostic value and biological function of miR-768-3p in breast cancer. The expression of miR-768-3p in tumor tissues and adjacent tissues of 116 patients with breast cancer obtained by surgery and normal breast cell lines MCF-10A and breast cancer cell lines (MCF-7, MDA-MB-231, T-47D and SK-BR-3) were detected by reverse transcription-quantitative PCR. The association between miR-768-3p expression and the clinicopathological characteristics of patients was analyzed using the χ2 test. In addition, the Kaplan-Meier method was used for survival analysis. A Cox regression model was used to examine the effect of miR-768-3p on the prognosis of patients with breast cancer. Hemocytometer cell counting and Transwell assays were used to detect the effects of miR-768-3p on the characteristbreast cancer. All experiments confirmed that miR-768-3p, a tumor suppressor, inhibited the viability, migration and invasion of breast cancer cells through eIF4E. miR-768-3p may be a potential prognostic marker of breast cancer and may participate in the progression of breast cancer.Colorectal cancer (CRC) is one of the most lethal malignances in humans. Hence, it is of great significance to identify regulatory molecules in CRC progression. Accumulating evidence has demonstrated that long non-coding RNAs (lncRNAs) are involved in cancer malignancy. It has been reported that long intergenic non-protein coding RNA 857 (LINC00857) acts as a vital oncogene in many types of cancer by promoting cell proliferation and migration. However, the role of LINC00857 in CRC remains unclear. In the present study, LINC00857 was upregulated in CRC tissue samples and cells. Next, in vitro loss-of-function experiments demonstrated that LINC00857 knockdown suppressed CRC cell viability, proliferation and migration, as well as epithelial-mesenchymal transition and increased cell apoptosis. Mechanistically, LINC00857 abundantly interacted with the RNA-binding protein YTH domain containing 1 (YTHDC1). YTHDC1 ultimately combined with solute carrier family 7 member 5 (SLC7A5) and increased SLC7A5 mRNA stability. Finally, a series of rescue experiments indicated that LINC00857 promoted the proliferation and migration of CRC cells by regulating mRNA stability. Thus, the present findings illustrated that LINC00857 functions as an oncogene in CRC cells via the YTHDC1/SLC7A5 axis.Colorectal cancer (CRC) is the third most common cancer worldwide. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 8 (SNHG8) acts as an oncogene in different types of cancer, including prostate, breast and ovarian cancer. read more SNHG8 promotes the tumorigenesis of CRC; however, its underlying molecular mechanism remains unclear. The present study aimed to explore the mechanism of SNHG8 on CRC development via various assays, including western blot, pull-down, PCR and immunofluorescence assays. The results of the present study demonstrated that SNHG8 expression was substantially upregulated in primary tumor tissues from The Cancer Genome Atlas dataset. Western blot and immunofluorescence analyses demonstrated that SNHG8 facilitated cell proliferation and autophagy in CRC cells. Notably, the function of SNHG8 in enhancing autophagy was dependent on autophagy-related gene 7 (ATG7). In addition, western blot analysis indicated that the effect of SNHG8 on autophagy in CRC cells was dependent on the miR-588/ATG7 axis. Taken together, the results of the present study suggest that SNHG8 promotes autophagy in CRC cells.Obg-like ATPase 1 (OLA1) is upregulated in the tumor tissues in different types of cancer. However, the function of OLA1 and its molecular mechanisms in endometrial cancer (EC) remain unknown. The present study aimed to elucidate OLA1 expression level and its biological function in endometrial cancer. The differential expression of OLA1 between EC tissues and non-cancerous tissues was analyzed using The Cancer Genome Atlas database and clinical samples. The association between clinicopathological characteristics and OLA1 expression was analyzed using bioinformatics analysis. Cell proliferation, migration and invasion were analyzed by short interfering RNA-mediated knockdown experiments, Cell Counting Kit-8, 5-Ethynyl-2'-deoxyuridine incorporation, wound healing, Transwell and Boyden assays. The potential signaling pathways associated with OLA1 in endometrial cancer were evaluated by Gene Set Enrichment Analysis. The expression levels of OLA1 in EC tissues were upregulated compared with that in non-cancerous tissues (P less then 0.001). Furthermore, patients with worse survival were found to have higher OLA1 expression, and increased OLA1 expression in endometrial cancer associated with clinical stage (P less then 0.01), histological type (P less then 0.01), histological grade (P less then 0.01), menstrual status (P less then 0.01), cancer status (P less then 0.05) and distant metastasis (P less then 0.05). In RL95-2 and HEC-1B cell lines, decreased levels of OLA1 inhibited proliferation, invasion and migration, and the TGF-β signaling pathway, ubiquitin-mediated proteolysis and Wnt signaling pathway may be involved in these mechanisms. The present study revealed that OLA1 could be a potential prognostic indicator and therapeutic target in endometrial cancer, and that the TGF-β signaling, Wnt signaling and ubiquitin-mediated proteolysis pathways may be regulated by OLA1.Over the past half century, contact lenses have been investigated for their potential as drug delivery devices for ocular therapeutics. Hundreds of studies have been published in the pursuit of the most effective and efficient release strategies and methods for contact lens drug delivery. This paper provides a thorough overview of the various contact lens drug delivery strategies, with a specific, comprehensive focus on in vivo studies that have been published since the field began in 1965. Significant accomplishments, current trends, as well as future strategies and directions are highlighted. In vivo study analysis provides a straightforward perspective and assessment of method success and commercialization potential in comparison to benchtop, in vitro studies. Analysis of the majority of published work indicates in vitro and in vivo studies do not correlate with a correlation coefficient of 0.25, with many in vitro studies grossly overestimating drug release duration and not showing appreciable drug release control.