New insights into the correlations between circulating tumor cells and target organ metastasis

Abstract

Organ-specific metastasis is the primary cause of cancer patient death. The distant metastasis of tumor cells to specific organs depends on both the intrinsic characteristics of the tumor cells and extrinsic factors in their microenvironment. During an intermediate stage of metastasis, circulating tumor cells (CTCs) are released into the bloodstream from primary and metastatic tumors. CTCs harboring aggressive or metastatic features can extravasate to remote sites for continuous colonizing growth, leading to further lesions. In the past decade, numerous studies demonstrated that CTCs exhibited huge clinical value including predicting distant metastasis, assessing prognosis and monitoring treatment response et al. Furthermore, increasingly numerous experiments are dedicated to identifying the key molecules on or inside CTCs and exploring how they mediate CTC-related organ-specific metastasis. Based on the above molecules, more and more inhibitors are being developed to target CTCs and being utilized to completely clean CTCs, which should provide promising prospects to administer advanced tumor. Recently, the application of various nanomaterials and microfluidic technologies in CTCs enrichment technology has assisted to improve our deep insights into the phenotypic characteristics and biological functions of CTCs as a potential therapy target, which may pave the way for us to make practical clinical strategies. In the present review, we mainly focus on the role of CTCs being involved in targeted organ metastasis, especially the latest molecular mechanism research and clinical intervention strategies related to CTCs.

Extracellular vesicles derived from SARS-CoV-2 M-protein-induced triple negative breast cancer cells promoted the ability of tissue stem cells supporting cancer progression

“…Consistently, nonaggressive BCC treated with conditioned medium derived from MpEV-ATMSC showed the induced migration ( Figure 2A ), in vivo metastasis ( Figure 2C ) and stemness potency ( Figures 3A, B ) while reduced the proliferation ( Figure 2B ). Although proliferation is necessary for the initiation of primary tumors, growth inhibition plays an important role for the survival of tumor cells in the circulation and invasion to secondary organs, resulting to a malignant phenotype ( 59 , 60 ). Therefore, it is worthy for a further study to examine the correlation between the reduced proliferation and malignant phenotypes of non-aggressive BCC treated with conditioned medium from MpEV-ATMSC by clarifying the signaling pathways regulating proliferation of these cells.…”

Advancements in Circulating Tumor Cell Research: Bridging Biology and Clinical Applications

“…Metastatic events in cancer involve the spread of tumor cells from the primary to secondary sites, following a phenotypic transition from epithelial to mesenchymal phenotype, cancer cell invasion into circulation, dormancy, and colonization at distant sites [ 56 , 57 ]. CTCs can be released by aggressive and metastatic tumors into circulation, where they extravasate to other remote sites for continuous colonization, leading to the growth of further lesions [ 58 ]. Nonetheless, research suggests that CTCs can be shed from primary tumors at early stages of cancer, challenging the traditional view that metastasis occurs primarily in advanced disease [ 6 ].…”

The intricate interplay between cancer stem cells and cell-of-origin of cancer: implications for therapeutic strategies

“…In prostate cancer, CSCs expressing the bone-specific chemokine receptor CCR3 preferentially establish bone metastases (101). Lung metastasis in various cancers, including breast and colon cancer, has been linked to the expression of specific adhesion molecules and chemokine receptors on CSCs that facilitate their homing to the lung microenvironment (102,103).…”