Invasion and metastasis of tumour cells resistant to chemotherapy

Abstract

Metastatic tumours resistant to chemotherapy are the major cause of the clinical failure in the treatment of malignant diseases. It is observed often that drugs active against primary tumours do not exhibit the same efficacy towards metastatic tumour cells having modified signaling pathways. Among cellular factors involved in the development of the metastatic potential of multidrug resistant tumour cells are some oncoproteins, antiapoptotic proteins, mutated suppressor proteins, integrins and CD44 receptor. It was also demonstrated that numerous chemotherapeutics have the effect on the emergence of the metastatic potential and multidrug resistance (MDR) phenomenon of tumour cells. The results of numerous studies suggest that genes involved in the development of MDR and metastatic phenotype of tumour cells are regulated by the same signaling pathways. They lead to the activation of transcription factors e.g. HIF-1α, NF-κB, Ets1 and AP-1 controlling the expression of genes involved in the development of the metastatic potential of multidrug resistant tumour cells. The identification of key cellular factors responsible for the emergence of the metastatic potential of MDR tumour cells could lead to the development of new efficient strategies for the treatment of metastatic tumours resistant to the conventional chemotherapy.

Two Novel Long Noncoding RNAs – RP11-296E3.2 and LEF1-AS1can – Separately Serve as Diagnostic and Prognostic Bio-Markers of Metastasis in Colorectal Cancer

“…Extensive studies have proved that metastasis plays a major role in cancer multiple drug resistance (MDR) [15]. Therefore, we further explored the relationships between MDR and lncRNAs expression in 20 patients’ tissues using an ATP-based tumor chemosensitivity assay (ATP-TCA).…”

Downregulation of GPSM2 is associated with primary resistance to paclitaxel in breast cancer

“…Drug resistance in tumor cells is an important contributory factor to disease progression (29). Here, we examined the potential role of GPSM2 expression in breast cancer by silencing its expression.…”

HMGA2 promotes the migration and invasion of gallbladder cancer cells and HMGA2 knockdown inhibits angiogenesis via targeting VEGFA

“…In the present study, HMGA2 knockdown and overexpression downregulated and upregulated, respectively, the expression levels of both Ki67 and PCNA, suggesting that HMGA2 may promote GBC cell proliferation. The invasion and metastasis of malignant tumors has been discovered to contribute to chemotherapy failure and death in patients with cancer ( 35 ). The results of the wound healing and Transwell assays in the current study revealed that HMGA2 silencing attenuated the migratory and invasive abilities of GBC cells, whereas HMGA2 overexpression exhibited the opposite results.…”