Reduced LINC00467 Elevates microRNA-125a-3p to Suppress Cisplatin Resistance in Non-Small Cell Lung Cancer Through Inhibiting Sirtuin 6 and Inactivating the ERK1/2 Signaling Pathway

Xue, Feng; Yang, Chuan; Yun, Keli; Jiang, Cailing; Ca, Rui; Liang, Ming; Wang, Quan; Bian, Weixin; Zhou, Hang; Liu, Zhipeng; Zhu, Lin

doi:10.2139/ssrn.3572847

Cited by 2 publications

(3 citation statements)

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“…Similarly, the difference in deletion mutation between the two groups was more pronounced in cell proliferation in the chemorefractory group (41). Interestingly, it has been indicated by some studies that inactivating the ERK1/2 signaling pathway would suppress cisplatin resistance in non-small cell lung cancer (42). It deeply supported the correlation of drug resistance and provided a basis for drug research and development.…”

Section: Discussionmentioning

confidence: 76%

Whole-Exome Sequencing Uncovers Specific Genetic Variation Difference Based on Different Modes of Drug Resistance in Small Cell Lung Cancer

Han

Zhao

et al. 2022

Front. Oncol.

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The poor survival rate of small cell lung cancer (SCLC) is mainly related to the condition that patients with SCLC often have good responses to first-line chemotherapy initially, but later on, most of these patients relapse rapidly due to resistance to further treatment. In this study, we attempted to analyze whole-exome sequencing data based on the largest sample size to date, to develop a classifier to predict whether a patient will be chemorefractory or chemosensitive and to explicate the risk of recurrence that affects the prognosis of patients. We showed the different characteristics of somatic mutational signatures, somatic mutation genes, and distinct genome instability between chemorefractory and chemosensitive SCLC patients. Amplified mutations in the chemosensitive group inhibited the regulation of the cell cycle process, transcription factor binding, and B-cell differentiation. Analysis of deletion mutation also suggested that detection of the chromosomal-level variation might influence our treatment decisions. Higher PD-L1 expressions (based on TPS methods) were mostly present among chemosensitive patients (p = 0.026), while there were no differences in PD-L1 expressions (based on CPS methods) and CD8+ TILs between the two groups. According to the model determined by logistic regression, each sample was endowed with a predictive probability value (PV). The samples were divided into a high-risk group (>0.55) and a low-risk group (≤0.55), and the survival analysis showed obvious differences between the two groups. This study provides a reference basis to translate this knowledge into practice, such as formulating personalized treatment plans, which may benefit Chinese patients with SCLC.

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Section: Discussionmentioning

confidence: 76%

Whole-Exome Sequencing Uncovers Specific Genetic Variation Difference Based on Different Modes of Drug Resistance in Small Cell Lung Cancer

Han

Zhao

et al. 2022

Front. Oncol.

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“…Linc00467 could also adsorb miR-20b-5p to relieve the inhibitory effect of miR-20b-5p on CCND1 to promote the growth of lung adenocarcinoma cells [25]. Additionally, it could bind miR-125a-3p to relieve the inhibitory effect of miR-125a-3p on SIRT6, thereby reducing the resistance of non-small cell lung cancer to cisplatin [29]. In cervical cancer, Linc00467 targets miR-107 to increase the expression of KIF23 to exert its cancer-promoting effect [23].…”

Section: Discussionmentioning

confidence: 99%

“…The regulatory mechanism of Linc00467 for human tumor development may be different for different types of tumors. Even for the same kind of tumor, the regulatory mechanism can differ [27][28][29].…”

Section: Introductionmentioning

confidence: 99%

The Role of Linc00467/TRAF5 in Promoting the Malignant Progression of Prostate Cancer and its Mechanism

Wang

Zhang

et al. 2022

Preprint

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Background Prostate cancer (PCa) is a commonly occurring cancer in the prostate. However, its pathogenesis is complex and remains largely unknown. This study aims to uncover the biological role of Linc00467/TRAF5 in influencing the progression of PCa and to provide novel directions for clinical treatment of PCa. Methods Linc00467 and TRAF5 were screened from PIA through chip detection in our previous study. Linc00467 and TRAF5 expression was verified using RT-qPCR in PC3, DU145, and normal human prostate epithelial cell line (HPrEC). Clinical specimens were collected to measure the expression of Linc00467 and TRAF5 in normal prostate tissue, PIA tissue, and PCa tissue using RT-qPCR. To further elucidate the regulatory effects of Linc00467 on TRAF5, siLinc00467 (SH4) was transfected into PCa cell lines (PC3 and DU145), and the expression of TRAF5 was detected by Western-blot. To study the impact of Linc00467 and TRAF5 on the biological behavior of PCa cells, we transfected siLinc00467 (SH4), overexpressed TRAF5 plasmid (Ov-TRAF5), and overexpressed siLinc00467 + TRAF5 plasmid into PC3 and DU145 cells, respectively. Next, we performed specific assays (MTT assay, scarification test, Transwell, Tunel, and flow cytometry) to analyze the effects of Linc00467 and TRAF5 on proliferation, migration, invasion, and apoptosis of PCa cells (PC3 and DU145). We also utilized a tumor-bearing nude mice model to understand the effects of Linc00467 and TRAF5 on tumor growth. Results The experimental results demonstrate that Linc00467 is highly expressed in PCa cell lines (PC3 and DU145), while the expression of TRAF5 is low. We found a similar pattern in clinical specimens (PIA and PCa tissues) where in Linc00467 was highly expressed and TRAF5 was downregulated. Inhibiting Linc00467 can promote TRAF5 expression, significantly reducing the proliferation, migration, and invasion of PCa cells (PC3 and DU145) and promoting apoptosis. The experiment on tumor-bearing nude mice showed that Linc00467 inhibition and overexpressed TRAF5 could inhibit tumor growth. Conclusion Our study suggests that Linc00467 is a tumor-promoting gene in PCa, while TRAF5 is a tumor suppressor gene. Furthermore, Linc00467 has a regulatory effect on TRAF5. The tumor-promoting effect of Linc00467 may be exerted by regulating TRAF5, but its specific mechanism needs to be explored further.

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Reduced LINC00467 Elevates microRNA-125a-3p to Suppress Cisplatin Resistance in Non-Small Cell Lung Cancer Through Inhibiting Sirtuin 6 and Inactivating the ERK1/2 Signaling Pathway

Cited by 2 publications

References 0 publications

Whole-Exome Sequencing Uncovers Specific Genetic Variation Difference Based on Different Modes of Drug Resistance in Small Cell Lung Cancer

Whole-Exome Sequencing Uncovers Specific Genetic Variation Difference Based on Different Modes of Drug Resistance in Small Cell Lung Cancer

The Role of Linc00467/TRAF5 in Promoting the Malignant Progression of Prostate Cancer and its Mechanism

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