Purpose:　Paraspeckle　component　1　(PSPC1)　is　upregulated　in　numerous　cancers　and　is　associated　with　reduced　patient　survival　rates.　Our　previous　research　indicated　that　elevated　PSPC1　levels　in　nasopharyngeal　carcinoma　(NPC)　are　positively　linked　to　radiation　resistance　and　tumor　metastasis,　two　primary　clinical　challenges　in　NPC　treatment.　However,　the　precise　role　of　PSPC1　in　radiation　resistance　and　metastasis　of　NPC　cells　remains　unclear.　This　study　aimed　to　explore　the　molecular　mechanisms　by　which　PSPC1　influences　radiation　resistance　and　metastasis　in　NPC.　Methods:　Using　the　radiation-resistant　R743　and　radiosensitive　CNE2　cell　lines　of　NPC,　we　examined　the　impact　of　PSPC1　expression　on　post-radiation　survival,　cell　cycle　progression,　apoptosis,　migration,　invasion,　and　tumor　growth.　CRISPR/Cas9　genome　editing　was　employed　to　generate　PSPC1　knockout　(KO)　lines　in　R743　cells,　while　PSPC1　overexpression　(pcD-PSPC1)　was　achieved　in　CNE2　cells　via　pcDNA3.1(+)-PSPC1　plasmid　transfection.　Results:　PSPC1　knockout　converted　R743　cells　from　radioresistant　to　radiosensitive,　whereas　PSPC1　overexpression　decreased　radiosensitivity　in　CNE2　cells.　Cell　cycle　analysis　revealed　that　PSPC1　KO　arrested　R743　cells　in　the　G2/M　phase　post-irradiation,　while　PSPC1　overexpression　prevented　G2/M　phase　arrest　in　CNE2　cells.　PSPC1　KO　increased　irradiation-induced　apoptosis　in　R743　cells,　whereas　PSPC1　overexpression　decreased　it　in　CNE2　cells.　Post-radiation,　PSPC1　KO　cells　showed　significantly　reduced　migration　and　invasion　abilities.　Bioinformatics　analysis　identified　SFPQ　as　a　PSPC1-interacting　protein,　with　PSPC1　KO　resulting　in　SFPQ　downregulation.　Additionally,　PSPC1　KO　enhanced　the　radiosensitivity　of　xenografted　tumors　in　nude　mice.　Conclusion:　Our　findings　suggest　that　PSPC1　is　a　pivotal　factor　in　enhancing　the　survival　and　spread　of　NPC　cells　post-radiation.　Targeting　PSPC1　or　its　downstream　pathways　could　offer　novel　strategies　to　overcome　radiation　resistance　and　metastasis　in　NPC　cells.