Due to Warburg effect, cancer cells prefer to metabolize glucose through aerobic glycolysis, which results in low efficiency of ATP production. It is reasonable to believe that tumor cells will rely more heavily on glucose uptake to make up insufficient energy produced from glycolysis. It is expected that, under glucose starvation, cancer cells will subject to more cell death than normal cells. Yet, even those solid tumors that are intermittently or constantly exposed to glucose deprivation were shown to grow vigorously. How tumors successfully cope with the glucose stress remains unclear. Metabolic reprogramming can be one of the key strategies by which cancer cells stay healthy under stresses. Tumor suppressor p53 was found to be mutated in about 50% of the human cancers and whether WT p53 in the remaining 50% tumors is tumor-preventing or tumor provoking is as yet an unanswered question. Recently, some reports have shown that p53 promotes cell survival under glucose stress. In this regard, p53 no longer acts as a tumor suppressor, rather it become an "accessory" to help cancer cells to survive harsh environment. Moreover, besides protein factors, whether and how p53 regulated lncRNA (s) is (are) involved in cancer cell death regulation has (have) been less studied. Here, we report a new p53-regulated lncRNA, which we named TRINGS (Tp53-regulated inhibitor of necrosis under glucose starvation), and it protects cancer cells from necrosis. A detailed mechanism of how TRINGS protects cancer cell against necrosis had also been delineated in this study. Here, we show that under glucose starvation condition, p53 directly upregulates lncRNA-TRINGS that in turn binds to STRAP and inhibits STRAPGSK3b-NFkB necrotic signaling axis, thus to protect tumor cells from necrotic cell death. Interestingly, TRINGS responses to glucose starvation, but not FBS-, serine-or glutamine-deprivation. Furthermore, its protective role is limited to tumor but not normal cells. Our finding reveals a p53-dependent, a long non-coding RNA TRINGS-mediated new necrotic pathway that contributes to survival of cancer cells harboring wild-type p53 under glucose stress.