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SRY-box transcription factors (SOXs) are effective inducers for the formation of stem-like phenotypes. As a member of SOX family,  SOX9  (SRY-box transcription factor 9) has been reported to be highly expressed and exert oncogenic functions in multiple human cancers. In this study, we hypothesized that  SOX9  could regulate the function of cancer stem/initiating cells (CSCs) to further facilitate the progression of colorectal cancer (CRC). Then, stable transfection of shRNAs was used to silence indicated genes. Loss-of-function experiments were conducted to demonstrate the in vitro function of CRC cells. In vivo study was conducted to determine the changes in tumorigenesis and metastasis in vivo. Bioinformatics analyses and mechanistic experiments were employed to explore the downstream molecules. Presently, GEPIA data indicated that  SOX9  was upregulated in 275 COAD (colon adenocarcinoma) samples relative to 349 normal tissues. Besides, we also proved the upregulation of  SOX9  in CRC cell lines (HCT15, SW480, SW1116, and HT-29) compared to normal NCM-460 cells. Silencing of  SOX9  suppressed cell growth, stemness, migration, and invasion. Mechanistically, SOX9 activated the transcription of lncRNA phenylalanyl-tRNA synthetase subunit alpha antisense RNA 1 ( FARSA-AS1 ), while  FARSA-AS1  elevated  SOX9  in turn by absorbing  miR-18b-5p  and augmented  FARSA  via sequestering  miR-28-5p . Furthermore, loss of  FARSA-AS1  hindered malignant phenotypes in vitro and blocked tumor growth and metastasis in vivo. Notably, we testified that  FARSA-AS1  aggravated the malignancy in CRC by enhancing  SOX9  and  FARSA . Our study unveiled a mechanism of SOX9- FARSA-AS1 - SOX9 / FARSA  loop in CRC, which provides some clews of promising targets for CRC.

SOX9-activated FARSA-AS1 predetermines cell growth, stemness, and metastasis in colorectal cancer through upregulating FARSA and SOX9