Metabolic reprogramming is a newly emerged hallmark of cancer attaining a recent consideration as an essential factor for the progression and endurance of cancer cells. A prime event of this altered metabolism is increased glucose uptake and discharge of lactate into the cells surrounding constructing a favorable tumor niche. Several oncogenic factors help in promoting this consequence including, pyruvate kinase M2 (PKM2) a rate-limiting enzyme of glycolysis in tumor metabolism via exhibiting its low pyruvate kinase activity and nuclear moon-lightening functions to increase the synthesis of lactate and macromolecules for tumor proliferation. Not only its role in cancer cells but also its role in the tumor microenvironment cells has to be understood for developing the small molecules against it which is lacking with the literature till date. Therefore, in this present review, the role of PKM2 with respect to various tumor niche cells will be clarified. Further, it highlights the updated list of therapeutics targeting PKM2 pre-clinically and clinically with their added limitations. This upgraded understanding of PKM2 may provide a pace for the reader in developing chemotherapeutic strategies for better clinical survival with limited resistance.

代谢重编程是癌症的一个新出现的标志，最近被认为是癌细胞进展和耐受的重要因素。这种代谢改变的一个主要事件是葡萄糖摄取增加以及乳酸释放到构建有利肿瘤生态位周围的细胞中。多种致癌因素有助于促进这一结果，包括丙酮酸激酶 M2 (PKM2)，它是肿瘤代谢中糖酵解的限速酶，通过表现出较低的丙酮酸激酶活性和核月光功能来增加乳酸和大分子的合成，从而促进肿瘤增殖。不仅要了解它在癌细胞中的作用，而且还必须了解它在肿瘤微环境细胞中的作用，以开发针对它的小分子，这是迄今为止文献中所缺乏的。因此，在本综述中，将阐明 PKM2 对于各种肿瘤微环境细胞的作用。此外，它还强调了针对 PKM2 的临床前和临床治疗的更新列表及其额外的局限性。对 PKM2 的加深理解可能会为读者制定化疗策略提供一个步伐，以在有限的耐药性下实现更好的临床生存。