Szaryńska Magdalena, Olejniczak Agata, Kobiela Jarosław, Spychalski Piotr, Kmieć Zbigniew
Department of Histology, Medical University of Gdańsk, 80-210 Gdańsk; Gdańsk, Poland.
Department of General, Endocrine and Transplant Surgery, Invasive Medicine Center, Medical University of Gdańsk, 80-214 Gdańsk, Poland.
Oncol Lett. 2017 Dec;14(6):7653-7668. doi: 10.3892/ol.2017.7261. Epub 2017 Oct 23.
Colorectal cancer (CRC) is the third most frequent malignancy and represents the fourth most common cause of cancer-associated mortalities in the world. Despite many advances in the treatment of CRC, the 5-year survival rate of patients with CRC remains unsatisfactory due to tumor recurrence and metastases. Recently, cancer stem cells (CSCs), have been suggested to be responsible for the initiation and relapse of the disease, and have been identified in CRC. Due to their basic biological features, which include self-renewal and pluripotency, CSCs may be novel therapeutic targets for CRC and other cancer types. Conventional therapeutics only act on proliferating and mature cancer cells, while quiescent CSCs survive and often become resistant to chemotherapy. In this review, markers of CRC-CSCs are evaluated and the recently introduced experimental therapies that specifically target these cells by inducing CSC proliferation, differentiation and sensitization to apoptotic signals via molecules including Dickkopf-1, bone morphogenetic protein 4, Kindlin-1, tankyrases, and p21-activated kinase 1, are discussed. In addition, novel strategies aimed at inhibiting some crucial processes engaged in cancer progression regulated by the Wnt, transforming growth factor β and Notch signaling pathways (pyrvinium pamoate, silibinin, PRI-724, P17, and P144 peptides) are also evaluated. Although the metabolic alterations in cancer were first described decades ago, it is only recently that the concept of targeting key regulatory molecules of cell metabolism, such as sirtuin 1 (miR-34a) and AMPK (metformin), has emerged. In conclusion, the discovery of CSCs has resulted in the definition of novel therapeutic targets and the development of novel experimental therapies for CRC. However, further investigations are required in order to apply these novel drugs in human CRC.
结直肠癌(CRC)是全球第三大常见恶性肿瘤,也是癌症相关死亡的第四大常见原因。尽管CRC的治疗取得了许多进展,但由于肿瘤复发和转移,CRC患者的5年生存率仍不尽人意。最近,癌症干细胞(CSCs)被认为是该疾病发生和复发的原因,并已在CRC中被鉴定出来。由于其具有自我更新和多能性等基本生物学特性,CSCs可能是CRC和其他癌症类型的新型治疗靶点。传统疗法仅作用于增殖和成熟的癌细胞,而静止的CSCs存活下来并常常对化疗产生耐药性。在这篇综述中,评估了CRC-CSCs的标志物,并讨论了最近引入的实验性疗法,这些疗法通过包括Dickkopf-1、骨形态发生蛋白4、Kindlin-1、端锚聚合酶和p21活化激酶1等分子诱导CSC增殖、分化并使其对凋亡信号敏感,从而特异性地靶向这些细胞。此外,还评估了旨在抑制由Wnt、转化生长因子β和Notch信号通路调控的癌症进展中一些关键过程的新策略(双羟萘酸吡维铵、水飞蓟宾、PRI-724、P17和P144肽)。尽管几十年前就首次描述了癌症中的代谢改变,但直到最近,靶向细胞代谢关键调节分子(如沉默调节蛋白1(miR-34a)和AMPK(二甲双胍))的概念才出现。总之,CSCs的发现导致了CRC新型治疗靶点的定义和新型实验性疗法的开发。然而,为了将这些新型药物应用于人类CRC,还需要进一步的研究。