This　study　was　aimed　to　explore　if　lncRNA　MALAT1　would　modify　chemo-resistance　of　non-small　cell　lung　cancer　(NSCLC)　cells　by　regulating　miR-197-3p　and　p120　catenin　(p120-ctn).　Within　this　investigation,　we　totally　recruited　326　lung　cancer　patients,　and　purchased　4　NSCLC　cell　lines　of　A549,　H1299,　SPC-A-1　and　H460.　Moreover,　cisplatin,　adriamycin,　gefitinib　and　paclitaxel　were　arranged　as　chemotherapies,　and　half　maximal　inhibitory　concentration　(IC50)　values　were　calculated　to　evaluate　the　chemo-resistance　of　the　cells.　Furthermore,　mice　models　of　NSCLC　were　also　established　to　assess　the　impacts　of　MALAT1,　miR-197-3p　and　p120-ctn　on　tumor　growth.　Our　results　indicated　that　MALAT1　and　miR-197-3p　were　both　over-expressed　within　NSCLC　tissues　and　cells,　when　compared　with　normal　tissues　and　cells　(P　＜　0.05).　The　A549,　H460,　SPC-A-1　and　SPC-A-1　displayed　maximum　resistances　to　cisplatin　(IC50　=　15.70　mu　g/ml),　adriamycin　(IC50　=　5.58　mu　g/ml),　gefitinib　(96.82　mu　mol/L)　and　paclitaxel　(141.97　nmol/L).　Over-expression　of　MALAT1　and　miR-197-3p,　or　under-expression　of　p120-ctn　were　associated　with　promoted　viability　and　growth　of　the　cancer　cells　(P　＜　0.05),　and　they　could　significantly　strengthen　the　chemo-resistance　of　cancer　cells　(P　＜　0.05).　MALAT1　Wt　or　p120-ctn　Wt　co-transfected　with　miR-197-3p　mimic　was　observed　with　significantly　reduced　luciferase　activity　within　NSCLC　cells　(P　＜　0.05).　Finally,　the　NSCLC　mice　models　were　observed　with　larger　tumor　size　and　weight　under　circumstances　of　over-expressed　MALAT1　and　miR-197-3p,　or　under-expressed　p120-ctn　(P　＜　0.05).　In　conclusion,　MALAT1　could　alter　chemo-resistance　of　NSCLC　cells　by　targeting　miR-197-3p　and　regulating　p120-ctn　expression,　which　might　assist　in　improvement　of　chemo-therapies　for　NSCLC.