LncRNA OTUD6B-AS1 promotes paclitaxel resistance in triple negative breast cancer by regulation of miR-26a-5p/MTDH pathway-mediated autophagy and genomic instability

Li, Rongguo; Huang, Yuqing; Lu, Jin-Pian; Zhang, Weijun; Wang, Zhenyu

doi:10.18632/aging.203672

Cited by 49 publications

(30 citation statements)

References 45 publications

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“…We found that lncRNA-mediated expression of autophagyassociated proteins promotes trastuzumab resistance in HER-2-positive breast cancer [63,64]. Li et al found that the OTUD6B-AS1/miR-26a-5p/MTDH signaling pathway promotes autophagy, thereby promoting the occurrence of paclitaxel resistance in triple-negative breast cancer [83]. These findings provide new insights into lncRNA-mediated autophagy as therapeutic methods for breast cancer.…”

Section: The Therapeutic Potentials and The Relevant Mechanisms Assoc...mentioning

confidence: 81%

“…Li et al found that miR-26a-5p is a protective element to protect breast cancer from attack, in contrast, OTUD6B-AS1 and MTDH are destructive elements of breast cancer, and miR-26a-5 is down-regulated through OTUD6B-AS1/miR-26a5p/MTDH pathway. MTDH and OTUD6B-AS1 overexpression promote autophagy and DNA damage, and autophagy defects can increase the short-term sensitivity of tumor cells to chemotherapeutic drugs [83]. In conclusion, OTUD6BAS1/miR-26A-5p/MTDH promotes PTX resistance in triple-negative breast cancer by upregulation of autophagy and DDR inhibition mediated genomic instability.…”

Section: Paclitaxelmentioning

confidence: 84%

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Crucial Roles of LncRNAs-Mediated Autophagy in Breast Cancer

Han¹,

Mo²,

Yang³

et al. 2022

Int. J. Med. Sci.

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Breast cancer remains a worldwide public health issue. LncRNA and autophagy respectively or simultaneously, get involved in cellular and molecular processes of many different cancers, including genesis, metastasis, and deterioration of breast cancer and other malignant tumors. In this review, relevant studies have been summarized, and we have found that lncRNA-mediated autophagy in luminal A breast cancer, luminal B breast cancer, HER-2 positive breast cancer, and basal-like breast cancer may play an important role in mediating drug resistance sensitivity. LncRNAs target genes and affect different signaling pathways to a complex network, which attenuates the occurrence and development of primary breast cancer by coordinating autophagy. Abnormal expression of LncRNA may lead to dysregulation of autophagy, resulting in tumor genesis, expansion, and resistance to anti-tumor therapy. Targeting specific lncRNAs for autophagy regulation may conduct as a bio-marker for reliable diagnosis and prognosis treatment of breast cancer or provide a promising therapeutic strategy.

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Section: The Therapeutic Potentials and The Relevant Mechanisms Assoc...mentioning

confidence: 81%

Section: Paclitaxelmentioning

confidence: 84%

Crucial Roles of LncRNAs-Mediated Autophagy in Breast Cancer

Han¹,

Mo²,

Yang³

et al. 2022

Int. J. Med. Sci.

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“… 20 , 21 , 22 , 23 On the other hand, OTUD6B‐AS1 promotes hepatocellular carcinoma cells proliferation and invasion and induces chemoresistance in breast cancer cell and cervical cancer cell. 24 , 25 , 26 How to make a wide use of OTUD6B‐AS1 is worth exploring and may provide a novel strategy to cancer treatment. The diversity of the composition of immune cell may promote tumor development and influence the response to therapy.…”

Section: Discussionmentioning

confidence: 99%

“…OTUD6B‐AS1 suppresses viability, migration and invasion in thyroid carcinomas, colorectal cancer cell and renal cell carcinoma 20–23 . On the other hand, OTUD6B‐AS1 promotes hepatocellular carcinoma cells proliferation and invasion and induces chemoresistance in breast cancer cell and cervical cancer cell 24–26 . How to make a wide use of OTUD6B‐AS1 is worth exploring and may provide a novel strategy to cancer treatment.…”

Section: Discussionmentioning

confidence: 99%

“…[20][21][22][23] On the other hand, OTUD6B-AS1 promotes hepatocellular carcinoma cells proliferation and invasion and induces chemoresistance in breast cancer cell and cervical cancer cell. [24][25][26] How to make a wide rapid progression and inefficient response to immunotherapy. 28 Yang et al indicated that the inhibition of ACAT1 (known as a key enzyme in lipid metabolism) contributes to the increase in plasma membrane, which leads to the proliferation of CD8 + T cells via enhancing T-cell receptor aggregation and signal transduction.…”

Section: Discussionmentioning

confidence: 99%

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A novel prognostic model associated with the overall survival in patients with breast cancer based on lipid metabolism‐related long noncoding RNAs

Shi

Zhou

Zhu³

et al. 2022

Clinical Laboratory Analysis

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Background Lipid metabolism is closely related to the occurrence and development of breast cancer. Our purpose was to establish a novel model based on lipid metabolism‐related long noncoding RNAs (lncRNAs) and evaluate the potential clinical value in predicting prognosis for patients suffering from breast cancer. Methods RNA data and clinical information for breast cancer were obtained from the cancer genome atlas (TCGA) database. Lipid metabolism‐related lncRNAs were identified via the criteria of correlation coefficient | R 2 | > 0.4 and p < 0.001, and prognostic lncRNAs were identified to establish model through Cox regression analysis. The training set and validation set were established to certify the feasibility, and all samples were separated into high‐risk group or low‐risk group. Gene Ontology (GO) and Gene Set Enrichment Analysis (GSEA) were conducted to evaluate the potential biological functions, and the immune infiltration levels were explored through Cibersortx database. Results A total of 14 lncRNAs were identified as protective genes (AC022150.4, AC061992.1, AC090948.3, AC092794.1, AC107464.3, AL021707.8, AL451085.2, AL606834.2, FLJ42351, LINC00926, LINC01871, TNFRSF14−AS1, U73166.1 and USP30−AS1) with HRs < 1 while 10 lncRNAs (AC022150.2, AC090948.1, AC243960.1, AL021707.6, ITGB2−AS1, OTUD6B−AS1, SP2−AS1, TOLLIP−AS1, Z68871.1 and ZNF337−AS1) were associated with increased risk with HRs >1. A total of 24 prognostic lncRNAs were selected to construct the model. The patients in low‐risk group were associated with better prognosis in both training set ( p < 0.001) and validation set ( p < 0.001). The univariate and multivariate Cox regression analyses revealed that risk score was an independent prognostic factors in both training set ( p < 0.001) and validation set ( p < 0.001). GO and GSEA analyses revealed that these lncRNAs were related to metabolism‐related signal pathway and immune cells signal pathway. Risk score was negatively correlated with B cells ( r = −0.097, p = 0.002), NK cells ( r = −0.097, p = 0.002), Plasma cells ( r = −0.111, p = 3.329e‐04), T‐cells CD4 ( r = −0.064, p = 0.039) and T‐cells CD8 ( r = −0.322, p = 2.357e‐26) and positively correlated with Dendritic cells ( r = 0.077, p = 0.013) and Monocytes ( r = 0.228, p = 1.107e‐13). Conclusion The prognostic model based on lipid metabolism lncRNAs possessed an impo...

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Targeting lncRNA DDIT4‐AS1 Sensitizes Triple Negative Breast Cancer to Chemotherapy via Suppressing of Autophagy

et al. 2023

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In this study, it is found that the lncRNA, DNA damage inducible transcript 4 antisense RNA1 (DDIT4-AS1), is highly expressed in triple-negative breast cancer (TNBC) cell lines and tissues due to H3K27 acetylation in the promoter region, and promotes the proliferation, migration, and invasion of TNBC cells via activating autophagy. Mechanistically, it is shown that DDIT4-AS1 induces autophagy by stabilizing DDIT4 mRNA via recruiting the RNA binding protein AUF1 and promoting the interaction between DDIT4 mRNA and AUF1, thereby inhibiting mTOR signaling pathway. Furthermore, silencing of DDIT4-AS1 enhances the sensitivity of TNBC cells to chemotherapeutic agents such as paclitaxel both in vitro and in vivo. Using a self-activatable siRNA/drug core-shell nanoparticle system, which effectively deliver both DDIT4-AS1 siRNA and paclitaxel to the tumor-bearing mice, a significantly enhanced antitumor activity is achieved. Importantly, the codelivery nanoparticles exert a stronger antitumor effect on breast cancer patient-derived organoids. These findings indicate that lncRNA DDIT4-AS1-mediated activation of autophagy promotes progression and chemoresistance of TNBC, and targeting of DDIT4-AS1 may be exploited as a new therapeutic approach to enhancing the efficacy of chemotherapy against TNBC.

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LncRNA OTUD6B-AS1 promotes paclitaxel resistance in triple negative breast cancer by regulation of miR-26a-5p/MTDH pathway-mediated autophagy and genomic instability

Cited by 49 publications

References 45 publications

Crucial Roles of LncRNAs-Mediated Autophagy in Breast Cancer

Crucial Roles of LncRNAs-Mediated Autophagy in Breast Cancer

A novel prognostic model associated with the overall survival in patients with breast cancer based on lipid metabolism‐related long noncoding RNAs

Targeting lncRNA DDIT4‐AS1 Sensitizes Triple Negative Breast Cancer to Chemotherapy via Suppressing of Autophagy

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