The occurrence of tumor cells is generally governed by the cluster of cells known as cancer stem cells, which are based on the informative model of cancer tissue consisting of stem cells that do have characteristics like auto-renewal activity and also provide intrinsic mechanisms for survival which are responsible for resistance against tumor cells to most of the drugs used in chemotherapy to cure cancer. During the course of therapy, it is difficult to eliminate CSCs due to which recurrence of tumor and metastasis develops inside the cell. Ongoing studies provide significant information on the particular phenotypic characteristics of cancer stem cells from different tumor types, as well as the signaling system and molecules that undergo auto-renewal and drug resistance. NPs (natural products), which are derivative of botanicals and food sources, may alter important signalling pathways that are involved in the perpetuation of CSC phenotypic traits. The chapter deals with the use of plant products to cure CSCs and their functioning.
TopIntroduction
In recent year’s various diagnostic and treatment technologies like radiotherapy, antineoplastic and chemotherapeutic drugs not only have made many solid tumors cure possible but also have given a new ray of hope to those people who are diagnosed with cancer. Although in numerous cases of cancer patients, the prognosis remains bleak because of the MDR (multiple drug resistance) and the high cancer recurrence rate visualized after the initial treatments of chemotherapy. Specifically, the cancers that affect patient multiple organ systems, i.e., metastatic cancer, are very difficult to treat, and sometimes complete or partial surgical resection of patients multiple tissues is required. Possibly CSCs (cancer stem cells) will explain the shortcomings that exist in the established treatments like chemotherapy. Usually, these cancer stem cells are the small tumor cells population having the ability to form phenotypically diverse tumors, which can differentiate and self-renew (Ahmed et al., 2013).
CSCs are described as the TICs (tumor-initiating cells) group that might have stem cell-like features. However, it is not very much clear whether the tumor cell's plasticity allows other cells to turn into the stem cell and attain the ability to restate heterogeneous tumors. In the late 90s, it was Bonnet and Dick who first identified the CSCs' role in tumor formation (Bonnet and Dick, 1997). In their research studies, they have revealed that the subpopulation of CD34+/CD38- cells (from acute myeloid leukemia) forms tumors in immunodeficient NOD (nonobese diabetic)/SCID (severe combined immunodeficiency) mice with greater effectiveness than the subpopulation of CD38-/CD34+ cells. Because of the ability of cancer stem cells to divide unequally allows them to differentiate and self-renew to produce dissimilar tumors that contain multiple phenotypes were also recognized. After this research, the cancer stem cells hypothesis was carefully verified. The results suggest that these cancer stem cells play a vital role in the growth of tumors for various cancers (Marchand and Pinho, 2021). Which includes colorectal carcinoma (O’Brien et al., 2007), hepatocellular carcinoma (Suetsugu et al., 2006), breast carcinoma (Liu et al., 2021), neck squamous cell carcinoma (Picon and Guddati, 2021), lung carcinoma (Paterson et al., 2021), pancreatic carcinoma (Li et al., 2009), glioblastoma (Patrawala et al., 2005), and ovarian adenocarcinoma (Szotek et l., 2006) are among the others. According to the CSC (cancer stem cells) hypothesis model, the recurrence of cancer after the treatment is because of the higher CSCs resistance towards the cellular toxins. Whereas the current treatments have the ability to successfully remove the bulk portion of the tumor mass, but due to its ability, the remaining CSCs form fully developed new tumors from the few left cells or even from the one left cell.
These cancer stem cells are thought to show resistance to different treatments via a number of cellular mechanisms like the detoxifying enzymes, quiescence, and drug efflux pumps (Zhang et al., 2017). According to the reports, the higher CSCs population within the tumor was found subsequently linked to MDR (multiple drug resistance) and poor diagnosis for cancer suffering individuals (Lee et al., 2011). CSCs are assumed to start the development of metastatic tumors by undergoing epithelial-mesenchymal transition, migrating to different organs, and finally reattaching by MET.