A novel mitosis-associated lncRNA, MA-linc1, is required for cell cycle progression and sensitizes cancer cells to Paclitaxel

Bida, Or; Gidoni, Moriah; Ideses, Diana; Efroni, Sol; Ginsberg, Doron

doi:10.18632/oncotarget.4944

Cited by 42 publications

(47 citation statements)

References 56 publications

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“…One central property of tumor cells, cell cycle progression, is controlled by E2F transcription factors [18]. The multifunctional transcription factor E2F1 participates in the timely regulation of replication genes to promote G1/S transition, and has previously been shown to regulate the expression of various lncRNAs [19,[53][54][55][56]. We provide evidence that E2F1 could elevate LINC00673 levels in tumor cells.…”

Section: Discussionmentioning

confidence: 72%

Targeting LINC00673 expression triggers cellular senescence in lung cancer

et al. 2018

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Aberrant expression of noncoding RNAs plays a critical role during tumorigenesis. To uncover novel functions of long non-coding RNA (lncRNA) in lung adenocarcinoma, we used a microarray-based screen identifying LINC00673 with elevated expression in matched tumor versus normal tissue. We report that loss of LINC00673 is sufficient to trigger cellular senescence, a tumor suppressive mechanism associated with permanent cell cycle arrest, both in lung cancer and normal cells in a p53-dependent manner. LINC00673depleted cells fail to efficiently transit from G1-to S-phase. Using a quantitative proteomics approach, we confirm the modulation of senescence-associated genes as a result of LINC00673 knockdown. In addition, we uncover that depletion of p53 in normal and tumor cells is sufficient to overcome LINC00673-mediated cell cycle arrest and cellular senescence. Furthermore, we report that overexpression of LINC00673 reduces p53 translation and contributes to the bypass of Ras-induced senescence. In summary, our findings highlight LINC00673 as a crucial regulator of proliferation and cellular senescence in lung cancer. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 72%

Targeting LINC00673 expression triggers cellular senescence in lung cancer

et al. 2018

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“…Regarding the PTX resistance in chemotherapy, various lncRNAs have been identified, including ma-linc1, n375709, NEAT1, and CCAT1 and so on. 8,[30][31][32] However, the function of FER1L4 in PTX resistance has not been clearly elucidated yet. But we discovered similar results to previous studies on the influence of FER1L4 on cell viability and apoptosis, which were evaluated in our experiments as PTX resistance reaction indicators.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of the lncRNA FER1L4 inhibits paclitaxel tolerance of ovarian cancer cells via the regulation of the MAPK signaling pathway

Liu

Zou

Tian

et al. 2018

J of Cellular Biochemistry

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To determine how the lncRNA FER1L4 in ovarian cancer cells influences paclitaxel (PTX) resistance, we examined the expression level of FER1L4 in human ovarian epithelial cell lines IOSE80 and HOSEpiC and human ovarian cancer cell lines OVCAR‐3, Caov‐3, and SKOV3 through RNA isolation and quantitative polymerase chain reaction (qRT‐PCR). SKOV3 cell lines were treated with PTX. The cell survival rate and apoptosis rate of SKOV3 and SKOV3‐PR at different PTX dose levels were evaluated. Next, qRT‐PCR was performed to detect the expression of FER1L4 in SKOV3 and SKOV3‐PR cell lines. SKOV3‐PR cell lines were transfected with pcDNA3.1 as the control group (SKOV3‐PR/pcDNA3.1) or pcDNA3.1‐FER1L4 to upregulate the expression level of FER1L4 (SKOV3‐PR/pcDNA3.1‐FER1L4). The level of cell survival, apoptosis, and colony formation were compared between the two groups using MTT, flow cytometry analysis, and colony formation assay. To reveal the molecular mechanism, we measured the relative protein phosphorylation level of ERK and MAPK in SKOV3, SKOV3‐PR, SKOV3‐PR/pcDNA3.1, and SKOV3‐PR/pcDNA3.1‐FER1L4 groups using an enzyme‐linked immunosorbent assay. The effects of SB203580 (a p38 MAPK inhibitor) on PTX were also investigated to reveal the function of the MAPK pathway on the PTX tolerance of SKOV3. In comparison with normal ovarian epithelial cells, FER1L4 was downregulated. The FER1L4 level was decreased in human ovarian cancer cells with drug resistance than in common ovarian cancer cells. The upregulation of FER1L4 could promote the PTX sensitivity of ovarian cancer cells. The increased level of FER1L4 could suppress the PTX resistance of ovarian cancer cells through the inhibition of the MAPK signaling pathway.

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“…lncRNAs are larger than miRNAs and have more complex structure. Deregulated expression of lncRNA disrupts cellular physiology and then leads to pathology [26–28]. Thus, we suggest that lncRNAs may play crucial roles in many biological processes and are vital to the formation of earlobe keloids.…”

Section: Discussionmentioning

confidence: 99%

Expression Profile of Long Noncoding RNAs in Human Earlobe Keloids: A Microarray Analysis

Guo

Yan

et al. 2016

BioMed Research International

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Background. Long noncoding RNAs (lncRNAs) play key roles in a wide range of biological processes and their deregulation results in human disease, including keloids. Earlobe keloid is a type of pathological skin scar, and the molecular pathogenesis of this disease remains largely unknown. Methods. In this study, microarray analysis was used to determine the expression profiles of lncRNAs and mRNAs between 3 pairs of earlobe keloid and normal specimens. Gene Ontology (GO) categories and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to identify the main functions of the differentially expressed genes and earlobe keloid-related pathways. Results. A total of 2068 lncRNAs and 1511 mRNAs were differentially expressed between earlobe keloid and normal tissues. Among them, 1290 lncRNAs and 1092 mRNAs were upregulated, and 778 lncRNAs and 419 mRNAs were downregulated. Pathway analysis revealed that 24 pathways were correlated to the upregulated transcripts, while 11 pathways were associated with the downregulated transcripts. Conclusion. We characterized the expression profiles of lncRNA and mRNA in earlobe keloids and suggest that lncRNAs may serve as diagnostic biomarkers for the therapy of earlobe keloid.

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A novel mitosis-associated lncRNA, MA-linc1, is required for cell cycle progression and sensitizes cancer cells to Paclitaxel

Cited by 42 publications

References 56 publications

Targeting LINC00673 expression triggers cellular senescence in lung cancer

Targeting LINC00673 expression triggers cellular senescence in lung cancer

Overexpression of the lncRNA FER1L4 inhibits paclitaxel tolerance of ovarian cancer cells via the regulation of the MAPK signaling pathway

Expression Profile of Long Noncoding RNAs in Human Earlobe Keloids: A Microarray Analysis

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