Long Intergenic Non-Protein Coding RNA 173 in Human Cancers

Mao, Wei; Liao, Yi; Tang, Liling

doi:10.3390/cancers14235923

Cited by 6 publications

(8 citation statements)

References 73 publications

(127 reference statements)

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“…Some papers reported that HDAC2 has required for the recruitment of HDAC1 to the repressed HDAC2. 22 Figure 3 showed that HDAC2 was dispensable for HDAC1 binding to HDAC2-activated targets. Subsequently, nicotine binds to E2F in the nucleus to the cytosol through the inducing cell receptor protein, α7nAChR.…”

Section: Discussionmentioning

confidence: 99%

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Cisplatin‐resistance induces lung squamous carcinoma cell growth by nicotine‐mediated α7nAchR/HDAC1/Cyclin D1/pRb cell cycle activation

Rao,

Guo,

2024

Cell Biochemistry & Function

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The majority of adenocarcinoma lung cancer is found in nonsmokers. A history of tobacco use is more common in squamous cell carcinoma of the lung. The aim of this study is to identify the cisplatin (CDDP)‐resistance that promotes lung squamous carcinoma cell growth through nicotine‐mediated HDAC1/7nAchR/E2F/pRb cell cycle activation. Squamous cell carcinoma (NCI‐H520 and NCI‐H157) cells were examined after cisplatin and nicotine treatment by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐2H‐tetrazolium bromide assay, cell migration assay, immunofluorescence staining, western blot analysis, and immunoprecipitation analysis. Consequently, CDDP is released from DNA and Rb phosphorylated pRb as a result of nicotine‐induced cancer cell proliferation through 7nAchR, which then triggers the opening of the HDAC1 cell cycle. The cell cycle is stopped when CDDP adducts are present. Nicotine exerts cancer cytoprotective effects by allowing HDAC1 repair mechanisms to re‐establish E2F promoting DNA stimulation cell cycle integrity in the cytosol and preventing potential CDDP and HDAC1 suppressed in the nuclear. Concentration expression of nicotine causes squamous carcinoma cell carcinogens to emerge from inflammation. COX2, NF‐KB, and NOS2 increase as a result of nicotine‐induced squamous carcinoma cell inflammation. Nicotine enhanced the cell growth‐related proteins such as α7nAchR, EGFR, HDAC1, Cyclin D, Cyclin E, E2F, Rb, and pRb by western blot analysis. It also induced cancer cell inflammation and growth. As a result, we suggest that nicotine will increase the therapeutic resistance effects of CDDP. This has the potential to interact with nicotine through α7nAchR receptors and HDAC1/Cyclin D/E2F/pRb potentially resulting in CDDP therapy resistance, as well as cell cycle‐induced cancer cell growth.

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Section: Discussionmentioning

confidence: 99%

“…A low concentration (1.0 µM) of nicotine has been reported to cause CDDP resistance. Some papers reported that HDAC2 has required for the recruitment of HDAC1 to the repressed HDAC2 22 . Figure 3 showed that HDAC2 was dispensable for HDAC1 binding to HDAC2‐activated targets.…”

Section: Discussionmentioning

confidence: 99%

Cisplatin‐resistance induces lung squamous carcinoma cell growth by nicotine‐mediated α7nAchR/HDAC1/Cyclin D1/pRb cell cycle activation

Rao,

Guo,

2024

Cell Biochemistry & Function

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“…It is known that lincRNAs affect biological pathways in autoimmune and neurodegenerative disorders [ 10 ], cardiovascular diseases [ 9 ], inflammation [ 11 , 12 ], and normal and malignant hematopoiesis [ 13 ]. LincRNAs are aberrantly expressed in various malignant tumors [ 14 ]. For example, aberrant expression of LINC00173 affects the initiation and progression of human cancers [ 15 ], while LINC01094 indirectly stabilizes the brain-derived neurotrophic factor via microRNA miR-577 in glioblastoma cells [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Long Intergenic Non-Coding RNAs of Human Chromosome 18: Focus on Cancers

Ershov,

Yablokov,

Mezentsev

et al. 2024

Biomedicines

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Malignant neoplasms are characterized by high molecular heterogeneity due to multilevel deregulation of gene expression and cellular functions. It is known that non-coding RNAs, including long intergenic non-coding RNAs (lincRNAs), can play significant roles in cancer biology. The current review focuses on a systematical analysis of genomic, transcriptomic, epigenomic, interactomic, and literature data on 65 lincRNAs of human chromosome 18 in the context of pan-cancer studies. The entire group of lincRNAs can be conditionally divided into 4 subgroups depending on experimental evidence on direct or indirect involvement in cancers and the biological associations with cancers, which we found during the data-mining process: the most studied (5 lincRNAs), moderately or poorly studied (11 lincRNAs), and understudied (31 lincRNAs). For the remaining 18 lincRNAs, data for analysis were fragmentary or missing. Among the key findings were the following: Of the lincRNAs of human chromosome 18, 40% have tissue-specific expression patterns, 22% of lincRNAs are known to have gene fusions, 40% of lincRNAs are prone to gene amplifications and/or deletions in cancers at a frequency greater than 3%, and 23% of lincRNAs are differentially expressed across cancer types, whereas 7% have subtype-specific expression patterns. LincRNAs’ interactomes consist of ‘master’ microRNAs and 47 proteins (including cancer-associated proteins and microRNAs) that can interact with 3 or more lincRNAs. Functional enrichment analysis of a set of highly co-expressed genes retrieved for 17 lincRNAs in different cancer types indicated the potential associations of these lincRNAs with cellular signaling pathways. Six lincRNAs encoded small open-reading frame (smORF) proteins with emerging roles in cancers, and microRNAs as well as proteins with known functions in molecular carcinogenesis can bind to coding regions of smORFs. We identified seven transcriptomic signatures with potential prognostic value, consisting of two to seven different lincRNAs only. Taken together, the literature, biomedical, and molecular biology data analyzed indicated that only five of all lincRNAs of human chromosome 18 are cancer-associated, while eleven other lincRNAs have the tendency to be associated with cancers.

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“…LINC00173 is associated with various types of human cancer in a cell context-dependent manner. It is involved in promoting tumorigenesis and tumor progression in squamous cell carcinoma, small cell lung cancer, hepatocellular carcinoma, and colorectal cancer [7]. In contrast, it also suppresses tumorigenesis and tumor progression in lung adenocarcinoma [8], cervical cancer [9], and acute myeloid leukemia [10].…”

Section: Introductionmentioning

confidence: 99%

“…In contrast, it also suppresses tumorigenesis and tumor progression in lung adenocarcinoma [8], cervical cancer [9], and acute myeloid leukemia [10]. This cell context-dependent action of LINC00173 can be attributed to its varied molecular functions; it acts as a molecular sponge of miRNAs to stabilize the mRNAs and enhance the expression of target genes [7], and it selectively binds to target proteins, such as DNMT1 [10] and HNRNPA2B1 [11], to modulate their downstream pathways. This variety of LINC00173 molecular actions indicates that LINC00173 may have as yet undiscovered functions in other important biological processes.…”

Section: Introductionmentioning

confidence: 99%

Expression of Tumor Suppressor FHIT Is Regulated by the LINC00173-SNAIL Axis in Human Lung Adenocarcinoma

Suzuki,

Sakai,

Ota

et al. 2023

IJMS

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Long non-coding RNAs (lncRNAs) play a critical role in a variety of human diseases such as cancer. Here, to elucidate a novel function of a lncRNA called LINC00173, we investigated its binding partner, target gene, and its regulatory mechanism in lung adenocarcinoma, including the A549 cell line and patients. In the A549 cell line, RNA immunoprecipitation (RIP) assays revealed that LINC00173 efficiently binds to SNAIL. RNA-seq and RT-qPCR analyses revealed that the expression of FHIT was decreased upon LINC00173 depletion, indicating that FHIT is a target gene of LINC00173. Overexpression of SNAIL suppressed and depletion of SNAIL increased the expression of FHIT, indicating that SNAIL negatively regulates FHIT. The downregulation of FHIT expression upon LINC00173 depletion was restored by additional SNAIL depletion, revealing a LINC00173-SNAIL-FHIT axis for FHIT regulation. Data from 501 patients with lung adenocarcinoma also support the existence of a LINC00173-SNAIL-FHIT axis, as FHIT expression correlated positively with LINC00173 (p = 1.75 × 10−6) and negatively with SNAIL (p = 7.00 × 10−5). Taken together, we propose that LINC00173 positively regulates FHIT gene expression by binding to SNAIL and inhibiting its function in human lung adenocarcinoma. Thus, this study sheds light on the LINC00173-SNAIL-FHIT axis, which may be a key mechanism for carcinogenesis and progression in human lung adenocarcinoma.

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Long Intergenic Non-Protein Coding RNA 173 in Human Cancers

Cited by 6 publications

References 73 publications

Cisplatin‐resistance induces lung squamous carcinoma cell growth by nicotine‐mediated α7nAchR/HDAC1/Cyclin D1/pRb cell cycle activation

Cisplatin‐resistance induces lung squamous carcinoma cell growth by nicotine‐mediated α7nAchR/HDAC1/Cyclin D1/pRb cell cycle activation

Long Intergenic Non-Coding RNAs of Human Chromosome 18: Focus on Cancers

Expression of Tumor Suppressor FHIT Is Regulated by the LINC00173-SNAIL Axis in Human Lung Adenocarcinoma

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