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Nasopharyngeal carcinoma (NC) poses a threat to the life of patients. Long non- coding RNA (LncRNA) is a novel kind of non-coding RNA, which plays a pivotal role through sponge microRNA (miRNA). Abnormal expression of small nucleolar RNA host gene 8 (SNHG8) is involved in various tumors; however, the role of SNHG8 in NC remains unknown. Quantitative real-time PCR (qRT-PCR) and Western blotting was employed to detect the expression levels of SNHG8, miR-588, and high mobility group A2 (HMGA2). Cell proliferation, migration, and invasion were analyzed by CCK-8 and transwell assays. miR-588 binding sites in SNHG8 were predicted by LncBase analysis. Luciferase reporter and RNA pull-down assay were used to confirm the interaction of SNHG8 and miR-588. SNHG8 was highly expressed in NC cells. The prognosis of the patients with NC in the high expression levels of SNHG8 was poorer than that in the low expression levels. The expression of SNHG8 was closely related to tumor size, TNM stage, and distal metastasis. Knockdown of SNHG8 inhibited cell proliferation, migration, and invasion of NC. SNHG8 targeted miR-588. Inhibition of miR-588 could partially reverse the knockdown of SNHG8 in NC cells, and miR-588 targeted HMGA2. In conclusion, SNHG8 promotes proliferation, migration, and invasion of NC cells through miR- 588/HMGA2 in NC as an oncogene. Key words: SNHG8, cell proliferation, cell migration and invasion, nasopharyngeal carcinoma, miR-588, HMGA2, oncogene. Le carcinome nasopharynge (CN) constitue une menace pour le pronostic vital des patients. L'ARN long non codant (LncRNA) est une nouvelle sorte d'ARN non codant, qui joue un role pivot par l'intermediaire du miARN eponge. L'expression anormale de SNHG8 joue un role dans diverses tumeurs. Cependant, le role de SNHG8 dans le CN demeure inconnu. A l'aide des techniques de PCR quantitatif par transcriptase inverse et d'immunobuvardage de Western, nous avons decele les taux d'expression de SNHG8, du miR-588 et de HMGA2. Nous avons etudie la proliferation, la migration et l'invasion des cellules a l'aide des epreuves CCK-8 et de transwell. Il etait possible de predire les sites de liaison du miR-588 avec SNHG8 a l'aide de l'analyse de la LncBase. A l'aide des epreuves de rapporteur par la luciferase et d'immunoprecipitation (<< pull-down >>) de l'ARN, nous avons confirme l'interaction entre SNHG8 et le miR-588. Les resultats ont montre que SNHG8 etait fortement exprime dans les cellules de CN. Le pronostic des patients atteints de CN presentant des taux d'expression de SNHG8 eleves etait moins favorable qu'avec de faibles taux d'expression. L'expression de SNHG8 etait etroitement liee a la taille de la tumeur, au stade TNM et a la presence de metastases a distance. La repression (<< knockdown >>) de SNHG8 permettait d'inhiber la proliferation, la migration et l'invasion des cellules de CN. SNHG8 ciblait le miR-588. L'inhibition du miR-588 pouvait inverser partiellement la repression de SNHG8 dans les cellules de CN. Le MiR-588 ciblait HMGA2. En conclusion, SNHG8 favorise la proliferation, la migration et l'invasion des cellules du CN par l'intermediaire du complexe miR-588/HMGA2 en tant qu'oncogene dans le CN. [Traduit par la Redaction] Mots-cles: SNHG8, proliferation, migration et invasion cellulaires, carcinome nasopharynge, miR-588, HMGA2, oncogene., Introduction Nasopharyngeal carcinoma (NC) is a malignant tumor that occurs at the top and side walls of the nasopharyngeal cavity. It is one of the malignant tumors with high incidence, [...]

SUMMARY Chlamydomonas reinhardtii, a unicellular green alga, has been widely used as a model organism for studies of algal, plant and ciliary biology. The generation of targeted amino acid mutations is often necessary, and this can be achieved using CRISPR/Cas9 induced homology‐directed repair to install genomic modifications from exogenous donor DNA. Due to the low gene editing efficiency, the technical challenge lies in identifying the mutant cells. Direct sequencing is not practical, and pre‐screening is required. Here, we report a strategy for generating and screening for amino acid point mutations using the CRISPR/Cas9 gene editing system. The strategy is based on designing donor DNA using codon degeneracy, which enables the design of specific primers to facilitate mutant screening by PCR. An in vitro assembled RNP complex, along with a dsDNA donor and an antibiotic resistance marker, was electroporated into wild‐type cells, followed by PCR screening. To demonstrate this principle, we have generated the E102K mutation in centrin and the K40R mutation in α‐tubulin. The editing efficiencies at the target sites for Centrin, TUA1, TUA2 were 4, 24 and 8% respectively, based on PCR screening. More than 80% of the mutants with the expected size of PCR products were precisely edited, as revealed by DNA sequencing. Subsequently, the precision‐edited mutants were biochemically verified. The introduction of codon degeneracy did not affect the gene expression of centrin and α‐tubulins. Thus, this approach can be used to facilitate the identification of point mutations, especially in genes with low editing rates. [ABSTRACT FROM AUTHOR]