Department of Pharmacy, COMSATS University Islamabad, Lahore Campus, Lahore, Pakistan.
Department of Clinical Sciences, Ajman University, Ajman, United Arab Emirates.
Pathol Oncol Res. 2021 Sep 13;27:1609828. doi: 10.3389/pore.2021.1609828. eCollection 2021.
A hormonal imbalance may disrupt the rigorously monitored cellular microenvironment by hampering the natural homeostatic mechanisms. The most common example of such hormonal glitch could be seen in obesity where the uprise in adipokine levels is in virtue of the expanding bulk of adipose tissue. Such aberrant endocrine signaling disrupts the regulation of cellular fate, rendering the cells to live in a tumor supportive microenvironment. Previously, it was believed that the adipokines support cancer proliferation and metastasis with no direct involvement in neoplastic transformations and tumorigenesis. However, the recent studies have reported discrete mechanisms that establish the direct involvement of adipokine signaling in tumorigenesis. Moreover, the individual adipokine profile of the patients has never been considered in the prognosis and staging of the disease. Hence, the present manuscript has focused on the reported extensive mechanisms that culminate the basis of poor prognosis and diminished survival rate in obese cancer patients.
激素失衡可能会通过干扰自然的体内平衡机制来破坏严格监测的细胞微环境。这种激素紊乱最常见的例子可以在肥胖中看到，脂肪细胞因子水平的上升是由于脂肪组织的膨胀。这种异常的内分泌信号会破坏细胞命运的调节，使细胞生活在支持肿瘤的微环境中。以前，人们认为脂肪细胞因子通过促进肿瘤的增殖和转移来支持癌症，而不直接参与肿瘤的转化和发生。然而，最近的研究报告了一些离散的机制，这些机制确立了脂肪细胞因子信号在肿瘤发生中的直接参与。此外，患者的个体脂肪细胞因子谱在疾病的预后和分期中从未被考虑过。因此，本论文集中讨论了已报道的广泛机制，这些机制是肥胖癌症患者预后不良和生存率降低的基础。
