Colorectal cancer (CRC) is a primary contributor to cancer-related mortality, largely due to its high metastatic potential. Although traditional treatments like surgery and chemotherapy have advanced, therapeutic resistance and relapse remain major challenges. Recent research has revealed that non-coding RNAs (ncRNAs) play pivotal roles in CRC progression, particularly by driving angiogenesis. Several classes of ncRNAs, including lncRNAs, miRNAs, and circRNAs, are key regulators of angiogenesis in CRC. For example, miRNAs such as miR-148a and miR-181a influence the VEGF and HIF-1α signaling pathways, which are critical for endothelial cell proliferation and migration. Certain lncRNAs, such as HNF1A-AS1 and UCA1, interact with miRNAs to modulate these pathways. CircRNAs (e.g., circ_0001821 and circ-ERBIN) often function as “miRNA sponges,” sequestering angiogenesis-inhibiting miRNAs to promote tumor vascularization. Furthermore, exosomes act as intercellular communication vesicles that transport ncRNAs (miRNAs, circRNAs) within the tumor microenvironment (TME). This process enables cancer cells to remodel their environment and facilitate metastatic dissemination. Specifically, exosomal ncRNAs, such as circ_0000467 and circ_0081069, can regulate angiogenesis-related pathways. This review integrates current findings on the complex interactions between miRNAs, lncRNAs, circRNAs, and exosomal ncRNAs in CRC angiogenesis. Understanding these molecular regulators highlights their potential as novel diagnostic biomarkers and therapeutic targets, which may lead to new targeted treatments that improve CRC patient outcomes by controlling angiogenesis and metastatic spread.

Purpose: Acute myeloid leukemia (AML) is known to be an invasive and highly lethal hematological malignancy in adults and children. Resistance to the present treatments, including radiotherapy and chemotherapy with their side effects and telomere length shortening are the main cause of the mortality in AML patients. Telomeres sequence which are located at the end of eukaryotic chromosome play pivotal role in genomic stability. Recent studies have shown that apoptosis process is blocked in AML patient by the excessive telomerase activity in cancerous blasts. Therefore, the find of effective ways to prevent disease progression has been considered by the researchers. Natural killer (NK) cells as granular effector cells play a critical role in elimination of abnormal and tumor cells. Given that the cytotoxic function of NK cells is disrupted in the AML patients, we investigated the effect of telomerase inhibitors on NK cell differentiation. Methods: To evaluate telomerase inhibition on NK cell differentiation, the expression of CD105, CD56, CD57, and KIRs was evaluated in CD34+ derived NK cells after incubation of them with BIBR1532. Results: The results showed that the expression of CD105, CD56, CD57, and KIRs receptors reduces after telomerase inhibition. According to these findings, BIBR1532 affected the final differentiation of NK cells. Conclusion: The results revealed that telomerase inhibitor drugs suppress cancer cell progression in a NK cells-independent process.