Abstract:Lung cancer is one of main causes of cancer mortality and 83% of lung cancer cases are classified as non-small cell lung cancer (NSCLC). Patients with NSCLC usually have a poor prognosis and one of the leading causes is drug resistance. With the progress of drug therapy, the emergence and development of drug resistance affected the prognosis of patients severely. Accumulating evidence reveals that long non-coding RNAs (lncRNAs), as "dark matters" of the human genome, is of great significance to drug resistance… Show more
“…However, we detected little variation in the phosphorylated-AKT and -ERK levels by siRNAs anti-SOX2-OT in NCI-H1975 cells. Therefore, our results support the hypothesis that LncRNAs are functional participants in therapy resistance/sensitivity to cancer-drugs, and target-gene therapies "EGFR/AKT/ERK/mTOR"[47]. It has been previously reported that SOX2-OT participates in the activation of the AKT-member of cellular signaling pathways in cholangiocarcinoma[14], as well as being involved in the magnitude of resistance mechanism to EGFR-TKIs-based treatment related to the functionality of phosphatase PTEN, reducing AKT phosphorylation in NSCLC[54].…”
Molecular model represents pieces of evidence, suggesting that LncRNA SOX2‐OT promotes AKT/ERK phosphorylation, as well as histone mark modifications (Activation H3K4me3/H3K27Ac versus Repression H3K9me3/H3K27me3) at GLI‐1 and SOX2‐OT gene promoter sequences (Likely SOX2) in a probable indirect manner (Dotted lines). Supporting that LncRNA SOX2‐OT is post‐translational and epigenetically involved in therapy resistance mechanisms, lung cancer malignancy, therapy resistance mechanisms, and clinical prognosis.
“…However, we detected little variation in the phosphorylated-AKT and -ERK levels by siRNAs anti-SOX2-OT in NCI-H1975 cells. Therefore, our results support the hypothesis that LncRNAs are functional participants in therapy resistance/sensitivity to cancer-drugs, and target-gene therapies "EGFR/AKT/ERK/mTOR"[47]. It has been previously reported that SOX2-OT participates in the activation of the AKT-member of cellular signaling pathways in cholangiocarcinoma[14], as well as being involved in the magnitude of resistance mechanism to EGFR-TKIs-based treatment related to the functionality of phosphatase PTEN, reducing AKT phosphorylation in NSCLC[54].…”
Molecular model represents pieces of evidence, suggesting that LncRNA SOX2‐OT promotes AKT/ERK phosphorylation, as well as histone mark modifications (Activation H3K4me3/H3K27Ac versus Repression H3K9me3/H3K27me3) at GLI‐1 and SOX2‐OT gene promoter sequences (Likely SOX2) in a probable indirect manner (Dotted lines). Supporting that LncRNA SOX2‐OT is post‐translational and epigenetically involved in therapy resistance mechanisms, lung cancer malignancy, therapy resistance mechanisms, and clinical prognosis.
“…4,5 Cisplatin (DDP) is a chemotherapeutic drug widely used in the treatment of lung cancer, but drug resistance of tumors had affected its application. 6 Exploring ways to reverse DDP drug resistance will improve the treatment of lung cancer.…”
Background: The incidence and mortality of lung cancer continue to increase around the world; in 2018, new lung cancer cases accounted for 11.6% of all cancer cases, and lung cancer deaths accounted for 18.4% of cancer deaths. Cisplatin (DDP) is a first-line chemotherapy drug for lung cancer; however, DDP resistance can lead to a poor prognosis in patients with lung cancer. Therefore, reversing DDP resistance is a treatment goal. Materials and Methods: Cell counting kit-8 (CCK8) assays, wound healing analyses, Transwell assays, in vitro tumor xenografts, and flow cytometry were used to detect the proliferation, migration, invasion, and apoptosis of multidrug resistant A549/DDP and PC9/ DDP cells, respectively. Western blot was performed to detect protein levels of cleaved caspase-3, CHOP, and GRP78. Results: Delicaflavone inhibited DDP resistance of lung cancer cells and decreased proliferation in a dose-and time-dependent manner. It also decreased migration and invasion and enhanced apoptosis. Western blots showed that delicaflavone overcame DDP resistance by increasing the expression of GRP78 and CHOP and the apoptosis-related protein cleaved caspase-3. Conclusion: Delicaflavone can reverse DDP resistance in A549/DDP and PC9/DDP cells by inhibiting cell proliferation and migration and enhancing apoptosis and cleaved caspase-3 levels by increasing the expression of CHOP and GRP78 protein via the endoplasmic reticular stress pathway. It could be a useful therapeutic adjunct to treat DDP-resistant lung cancer.
“…Among these non-coding genes, long non-coding RNAs (lncRNAs) are emerging as a new class of indispensable players involved in the tumorigenesis [ 3 , 5 , 6 ]. Moreover, the dysregulation of a number of lncRNA targets has been reported to associate with the stage and prognosis of many tumor types [ 7 , 8 ] including breast cancer [ 9 , 10 ], lung cancer [ 11 , 12 ], and liver cancer [ 13 , 14 ], as well as linked to resistance against chemotherapy and targeted therapy [ 15 , 16 ]. For example, the overexpression of the lncRNAHOX transcript antisense intergenic RNA(HOTAIR) promotes the metastasis of breast cancer cells [ 17 ].…”
Long noncoding RNAs (lncRNAs) have been found to associate with all major types of malignancies and play important roles in regulating several hallmarks of cancer by interacting with proteins, DNA, and RNA. The possible functions of lncRNAs and their roles in the regulation of tumour growth will be reported and discussed in the present review. In our recent report, based on genetic mice models and a series of systematic analyses, we suggested that lncRNAs also play critical roles in the regulation of antigen presentation in tumour cells and allow tumour cells to escape immune surveillance, which further broadens the scope of understanding lncRNA functions and how they relate to cancer immunotherapy resistance.
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