Telomere is the physical end of eukaryotic linear chromosome. It protects chromosomes from degradation and end-to-end fusion. Telomere composes of short, tandem, repeated sequences that are rich in G-residues. Due to the end replication problem, telomere cannot be fully replicated after each cycle of DNA synthesis. As a results, telomere length is shortened upon each cell division that eventually leads to cell growth arrest through activation of DNA damage response. This specific type of cell growth arrest is termed cellular senescence, which is considered as a hallmark of aging. Shortening of telomere length is the main cause to induce cellular senescence in most of the human somatic cells. To maintain proliferation capacity, cancer cells utilize two mechanisms to extend telomere lengths, telomerase and recombination. Telomerase is a ribonucleoprotein that utilizes its RNA component to extend telomeres. It is activated in ~85-90% of cancer cells. With the important role in maintaining proliferative capacity of cancer cells, telomerase is considered as a target for anti-cancer therapy. The potential of telomerase inhibitors in anti-cancer therapy will be discussed. Although the mechanisms of how telomerase is activated in cancer cells and how it extends telomere length are well studied, however, the mechanism of recombination-based telomere extension is less clear. Using yeast Saccharomyces cerevisiae as a model, we identified telomeric transcript TERRA has a role in regulating telomere recombination. The long non-coding RNA TERRA forms a R-loop structure to induce telomere recombination. The mechanistic detail of how TERRA is involved in telomere recombination will be discussed. In addition to cell growth arrest, senescent cells are also characterized by specific phenotypes such as enlarged cell size, activation of lysosomal β-galactosidase activity, formation of heterochromatin foci, and secretion of several cytokines. However, the mechanism of how senescent cells render these phenotypes is largely unknown. We applied both genomic and proteomic approaches to identify factors that are important for regulating these senescent phenotypes. The status of our current progress will be discussed.