lincâROR is reported to be a potential biomarker of breast cancer, but the detailed mechanism of lincâRORâmediated breast cancer regulation has not been fully studied. We aimed to explore how lincâROR affects proliferation, metastasis, and drug sensitivity in breast cancer. Cell lines in which lincâROR was overexpressed or knocked down were constructed, and the cell proliferation, colony formation, cell migration, and invasion abilities of these lines were explored. A CCKâ8 assay was performed to determine the sensitivity of the breast cancer cells to rapamycin. Nextâgeneration sequencing was conducted to explore the detailed regulatory mechanism of lincâROR; differentially expressed RNAs in the lincâRORâoverexpressing cell line compared with the negative control were screened out, and their target genes were chosen to perform Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes analysis, proteinâprotein interaction network analysis, and competing endogenous RNA (ceRNA) network analysis. The ceRNA mechanism of lincâROR for miRâ194â3p, which targets MECP2, was determined through dualâluciferase reporter assay, RTâqPCR, western blot, and rescue experiments. Finally, we found that lincâROR was upregulated in breast tumor tissues. lincâROR promoted the cell proliferation, colony formation, cell migration, and invasion of breast cancer and decreased the sensitivity of breast cancer cells to rapamycin. The overexpression of lincâROR triggered changes in the whole transcriptome of breast cancer cells, and a total of 85 lncRNAs, 414 microRNAs, 490 mRNAs, and 92 circRNAs were differentially expressed in the lincâRORâoverexpressing cell line compared with the negative control. Through a series of bioinformatic analyses, the âlincâROR/miRâ194â3p/MECP2â ceRNA regulatory axis was confirmed to be involved in the lincâRORâmediated progression and drug sensitivity of breast cancer. In conclusion, lincâROR serves as an oncoâlncRNA in breast cancer and promotes the survival of breast cancer cells during rapamycin treatment by functioning as a ceRNA sponge for miRâ194â3p, which targets MECP2.