Close interactions between lncRNAs, lipid metabolism and ferroptosis in cancer

Huang, Jingjing; Jin, Wang; He, Hua; Huang, Zichen; Wu, Sufang; Chen, Chao; Liu, Wenbing; Xie, Li; Tao, Yongguang; Li, Cong; Jiang, Yiqun

doi:10.7150/ijbs.66181

Cited by 41 publications

(23 citation statements)

References 225 publications

(257 reference statements)

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“…Accumulating evidence revealed that lncRNAs are essential for many cellular functions, including regulating gene expression and epigenetic signatures like cell viability, proliferation, and cell death ( Huang et al, 2021 ). Our earlier research demonstrated the critical functions of lncRNAs by showing their participation in the regulation of malignant biological behaviours and RCDs of cancer ( Mao et al, 2018 ; Wang et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Overexpression of LINC00551 promotes autophagy-dependent ferroptosis of lung adenocarcinoma via upregulating DDIT4 by sponging miR-4328

Xiong

Yang

Peng

et al. 2022

PeerJ

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According to mounting evidence, long noncoding RNAs (lncRNAs) play a vital role in regulated cell death (RCD). A potential strategy for cancer therapy involves triggering ferroptosis, a novel form of RCD. Although it is thought to be an autophagy-dependent process, it is still unclear how the two processes interact. This study characterized a long intergenic noncoding RNA, LINC00551, expressed at a low level in lung adenocarcinoma (LUAD) and some other cancers. Overexpression of LINC00551 suppresses cell viability while promoting autophagy and RSL-3-induced ferroptosis in LUAD cells. LINC00551 acts as a competing endogenous RNA (ceRNA) and binds with miR-4328 which up-regulates the target DNA damage-inducible transcript 4 (DDIT4). DDIT4 inhibits the activity of mTOR, promotes LUAD autophagy, and then promotes the ferroptosis of LUAD cells in an autophagy-dependent manner. This study provided an insight into the molecular mechanism regulating ferroptosis and highlighted LINC00551 as a potential therapeutic target for LUAD.

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Section: Introductionmentioning

confidence: 99%

Overexpression of LINC00551 promotes autophagy-dependent ferroptosis of lung adenocarcinoma via upregulating DDIT4 by sponging miR-4328

Xiong

Yang

Peng

et al. 2022

PeerJ

Self Cite

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“…These results suggest that ferroptosis may be regulated by different genes or non-coding RNAs in osteosarcoma, but the expression of these regulators differs in osteosarcoma and normal tissues. Notably, lncRNAs are closely associated with ferroptosis in cancer by mediating the expression of lipid metabolism-related enzymes and ferroptosis-related genes at multiple levels, including RNA splicing and post-transcriptional (41). For example, the lncRNA GABPB1-AS1 has been implicated in erastin-induced ferroptosis, which could increase ROS production and negatively affect cellular antioxidant capacity, thereby inhibiting hepatocellular carcinoma cell growth (79).…”

Section: Discussionmentioning

confidence: 99%

“…The FRL prognostic signature score, which we named “FRL-score,” was calculated as follows: FRL-score=Σ (βi × Expi) (β: coefficients, Exp: lncRNA expression level). Since few datasets are containing FRLs in osteosarcoma, we randomly divided the osteosarcoma patients with survival data in the TARGET database into a test set ( 41 ) and a training set ( 44 ) using the “caret” package ( 57 ). We constructed an FRL prognostic signature in the training set and validated it using the test set and the whole set.…”

Section: Methodsmentioning

confidence: 99%

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Comprehensive Analysis of a Ferroptosis-Related lncRNA Signature for Predicting Prognosis and Immune Landscape in Osteosarcoma

Zhang

Liu

et al. 2022

Front. Oncol.

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Research on the implications of ferroptosis in tumors has increased rapidly in the last decades. There are evidences that ferroptosis is involved in several aspects of cancer biology, including tumor progression, metastasis, immunomodulation, and therapeutic response. Nonetheless, the interaction between ferroptosis-related lncRNAs (FRLs) and the osteosarcoma immune microenvironment is poorly understood. In this study, a risk model composed of FRLs was developed using univariate and LASSO Cox regression analyses. On the basis of this model, FRL scores were calculated to systematically explore the role of the model in predicting the prognosis and immune characteristics of osteosarcoma patients. Survival analysis showed that osteosarcoma samples with lower FRL-score had better overall survival. After predicting the abundance of immune cells in osteosarcoma microenvironment by single-sample gene-set enrichment analysis (ssGSEA) and ESTIMATE analysis, we found that the FRL-score could distinguish immune function, immune score, stromal score, tumor purity, and tumor infiltration of immune cells in different osteosarcoma patients. In addition, FRL-score was also associated with immune checkpoint gene expression and half-maximal inhibitory concentration of chemotherapeutic agents. Finally, we confirmed that knockdown of RPARP-AS1 suppressed the malignant activity of osteosarcoma cells in vitro experiments. In general, the FRL-based prognostic signature could promote our understanding of the immune microenvironment characteristics of osteosarcoma and guide more effective treatment regimens.

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“…Lipid metabolism plays an important role in tumorigenesis and development [20,21]. During malignant progression, the availability of nutrients in the tumor microenvironment constantly changes and tumor cells utilize the lipid metabolism to sustain rapid proliferation and metastasis [22,23].…”

Section: Discussionmentioning

confidence: 99%

Downregulation of FABP5 suppresses mTOR -mediated autophagy via an increase in FASN to promote colorectal cancer progression

Chen

et al. 2022

Preprint

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BackgroundLipid metabolism plays an important role in the occurrence and development of cancer, in particular, digestive system tumors such as colon cancer. Here, we investigated the role of the fatty acid-binding protein 5 (FABP5) in colorectal cancer(CRC). MethodsTo this end, tissue microarray was initially used for analysis of FABP5 expression, followed by generation of stable cell lines with knockdown or overexpression of FABP5 for a series of functional assays including CCK-8, colony formation, EdU and transwell experiments. Co-IP, RNA-seq and omics-based lipid metabolism studies were further performed to explore the mechanisms of action of FABP5 in CRC. The function of FABP5 in vivo was analyzed with the aid of tumor xenograft and immunohistochemistry experiments. ResultsWe observed marked downregulation of FABP5 in CRC. Data from functional assays revealed inhibitory effects of FABP5 on cell proliferation, colony formation, migration, invasion as well as tumor growth in vivo. In terms of mechanistic insights, FABP5 interacted with fatty acid synthase (FASN) and activated the ubiquitin proteasome pathway, leading to a decrease in FASN expression and lipid accumulation, in turn, suppressing mTOR signaling and facilitating cell autophagy. Orlistat, a FASN inhibitor, exerted anticancer effects both in vivo and in vitro. Moreover, the upstream RNA demethylase ALKBH5 positively regulated FABP5 expression via an m 6 A-independent mechanism. ConclusionOur collective ndings offer valuable insights into the critical role of the FABP5/FASN axis in tumor progression and uncover a potential mechanism linking lipid metabolism to development of CRC, providing novel therapeutic targets for future interventions.

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Close interactions between lncRNAs, lipid metabolism and ferroptosis in cancer

Cited by 41 publications

References 225 publications

Overexpression of LINC00551 promotes autophagy-dependent ferroptosis of lung adenocarcinoma via upregulating DDIT4 by sponging miR-4328

Overexpression of LINC00551 promotes autophagy-dependent ferroptosis of lung adenocarcinoma via upregulating DDIT4 by sponging miR-4328

Comprehensive Analysis of a Ferroptosis-Related lncRNA Signature for Predicting Prognosis and Immune Landscape in Osteosarcoma

Downregulation of FABP5 suppresses mTOR -mediated autophagy via an increase in FASN to promote colorectal cancer progression

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