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PRPF6 promotes ovarian cancer metastasis and paclitaxel resistance by inducing alternative splicing of SNHG16 (downregulating SNHG16-L while upregulating SNHG16-S), where SNHG16-L inhibits GATA3 transcription through CEBPB binding, ultimately forming a PRPF6/SNHG16-L/CEBPB/GATA3 regulatory axis, with clinical correlations showing PRPF6 overexpression in chemoresistant OC tissues linked to advanced FIGO stages and poor therapeutic outcomes [114]