Y Chromosome LncRNA Are Involved in Radiation Response of Male Non–Small Cell Lung Cancer Cells

Brownmiller, Tayvia; Juric, Jamie A.; Ivey, Abby D.; Harvey, Brandon M.; Westemeier, Emily S.; Winters, Michael T.; Stevens, Alyson M.; Stanley, Alana N.; Hayes, Kevin; Sprowls, Samuel A.; Ammer, Amanda G.; Walker, Mackenzee; Bey, Erik A.; Xiao-liang, WU; Lim, Zuan Fu; Zhu, Lin; Wen, Sijin; Hu, Gangqing; Patrick, C.; Martínez, Iván

doi:10.1158/0008-5472.can-19-4032

Cited by 29 publications

(23 citation statements)

References 54 publications

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“…More than 50% of breast cancer patients would undergo radiotherapy during their course of treatment. Radiotherapy, in most cases, through X-ray ionizing radiation, inducing damage of DNA via directly or indirectly attacking the backbone of DNA and triggering a sequence of cellular response (12,48,49).…”

Section: Discussionmentioning

confidence: 99%

LncRNA FGD5-AS1 Facilitates the Radioresistance of Breast Cancer Cells by Enhancing MACC1 Expression Through Competitively Sponging miR-497-5p

Lei

Chen

et al. 2021

Front. Oncol.

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BackgroundLncRNA-FGD5-AS1, as an oncogene, participates in the development and progress of various cancers. However, the exact role and the molecular mechanisms by which FGD5-AS1 regulates radiosensitivity in breast cancer (BC) remains largely unknown.MethodsWe used X-Ray weekly-dose-increase method to establish radiation-resistance cell lines. Bioinformatics tools analyze the expression of FGD5-AS1 in breast cancer tissue and evaluated the relationship between FGD5-AS1 and clinic-pathological features. CCK-8 and colony formation were used to analyze cell proliferation. Western blotting and qPCR were applied to detect protein and gene expression, respectively. RNA interference was used to knock down the endogenous gene expression. Luciferase reporter system and immunoprecipitates were applied to verify the target of FGD5-AS1.ResultFGD5-AS1 was overexpressed in BC tissues and radiation-resistance cell lines. Higher levels of FGD5-AS1 predicted poorer clinical characteristics and prognosis. Loss-of-function FGD5-AS1 sensitized BC cells to X-ray, meanwhile, the cell gained radiation-resistance when exogenous FGD5-AS1 was expressed. FGD5-AS1 depletion arrested cells at G0/G1 and triggers cell apoptosis. The starBase database (ENCORI), predicted binding site of miR-497-5p in FGD5-AS1 sequence, and luciferase reporter system and immunoprecipitates verified miR-497-5p was the target of FGD5-AS1. Furthermore, MACC1 was predicted and verified as the target of miR-497-5p. Loss-of-function FGD5-AS1 sensitized ionizing radiation was rescued by the up-regulation of MACC1 and the inhibition of miR-497.ConclusionFGD5-AS1 displays an oncogene profile in CRC; patients with high expression of FGD5-AS1 should benefit less from radiotherapy and need a more frequent follow-up. Besides, FGD5-AS1 may be a potential therapeutic target for CRC.

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Section: Discussionmentioning

confidence: 99%

LncRNA FGD5-AS1 Facilitates the Radioresistance of Breast Cancer Cells by Enhancing MACC1 Expression Through Competitively Sponging miR-497-5p

Lei

Chen

et al. 2021

Front. Oncol.

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“…The lncRNA HOTAIRM1 was reported to be downregulated in papillary thyroid cancer, significantly associated with lymph node metastasis, TNM stage and better prognosis, and suppress cell growth, invasion and migration [27]. In addition, Brownmiller et al found a significant difference in the expression of the Y chromosome lncRNA linc-SPRY3-2/3/4 between radiation-sensitive and radiation-resistant non-small cell lung cancer cells, and confirmed that knockdown of linc-SPRY3-2/3/4 promoted cell viability and resistance to apoptosis after treatment with 8 Gy [28]. In this study, we found that LINC00958 was upregulated in colorectal cancer tissues, which was in accordance with a previous study [29].…”

Section: Discussionmentioning

confidence: 86%

Long noncoding RNA LINC00958 suppresses apoptosis and radiosensitivity of colorectal cancer through targeting miR-422a

et al. 2021

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Background Long noncoding RNAs (lncRNAs) have been elucidated to participate in the development and progression of various cancers. In this study, we aimed to explore the underlying functions and mechanisms of LINC00958 in colorectal cancer. Methods LINC00958 expression in colorectal cancer tissues was examined by qRT-PCR. The correlations between LINC00958 expression and clinical characteristics and prognosis were evaluated. The biological functions of LINC00958 were detected by CCK-8, MTT, colony formation and flow cytometric analyses. RNA pulldown, RIP and luciferase reporter assays were used to confirm the regulatory effects of LINC00958 on miR-422a. Rescue experiments were performed to detect the effects of miR-422a on the roles of LINC00958. Results LINC00958 was upregulated in colorectal cancer tissues and cell lines. High LINC00958 levels were positively associated with T stage and predicted poor prognosis. Cell experiments showed that LINC00958 promoted cell proliferation and suppressed apoptosis and sensitivity to radiotherapy in vitro and promoted tumor growth in vivo. Bioinformatics analysis predicted the binding site of miR-422a on LINC00958. Mechanistically, RNA pulldown, RIP and luciferase reporter assays demonstrated that LINC00958 specifically targeted miR-422a. In addition, we found that miR-422a suppressed MAPK1 expression by directly binding to the 3’-UTR of MAPK1, thereby inhibiting cell proliferation and enhancing cell apoptosis and radiosensitivity. Furthermore, miR-422a rescued the roles of LINC00958 in promoting MAPK1 expression and cell proliferation and decreasing cell apoptosis and radiosensitivity. Conclusions LINC00958 promoted MAPK1 expression and cell proliferation and suppressed cell apoptosis and radiosensitivity by targeting miR-422a, which suggests that it is a potential biomarker for the prognosis and treatment of colorectal cancer.

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“…For example, lncRNA CRNDE/PRC2 targeting p21 enhance radio-resistance of NSCLC [24]. A recent study revealed that linc-SPRY3-2/3/4, Y chromosome non-coding RNA, regulated radiation sensitivity and affected apoptosis and cell viability in NSCLC [25]. LncRNA PVT1 de ned as a poor prognosis factor, enhances radio-resistance by regulating cell apoptosis in nasopharyngeal carcinoma [26].…”

Section: Discussionmentioning

confidence: 99%

Silencing of lncRNA H19 Enhances the Sensitivity to X-rays and Carbon-Ions Through the miR-130a-3p /WNK3 Signal Axis in Non-Small-Cell Lung Cancer Cells

Zhao

Jin

Zhang

et al. 2021

Preprint

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Background: LncRNA H19 was believed to act as an oncogene in various types of tumors and was considered to be a therapeutic target and diagnosis marker. However, the role of lncRNA H19 in regulating the radiosensitivity of non-small cell lung cancer (NSCLC) cells was unknown. However, the effects of lncRNA H19 on radiosensitivity of NSCLC were not clear. Methods: The expression profiles of lncRNAs were explored via transcriptome sequencing in NSCLC. The CCK-8, EDU, and clonogenicity survival assay were conducted to explore the proliferation and radiosensitivity in NSCLC cells. Results: Expression patterns of lncRNAs revealed that compared with A549 cells, lncRNA H19 was upregulated in radioresistant NSCLC(A549-R11) cells. Knockdown experiments revealed that lncRNA H19 enhanced the radiation sensitivity of both A549 and H460 cancer cell lines to X-rays and carbon ion irradiation. Mechanistically, lncRNA H19 upregulated With-No-Lysine Kinase 3 (WNK3) expression via serving as a sponge of miR-130a-3p and promoted the resistance of NSCLC cells to both X-rays and carbon ion irradiation. Conclusion: Knockdown of lncRNA H19 promoted the radiation sensitivity of NSCLC cells to X-rays and carbon ion irradiation. Hence, lncRNA H19 might function as a potential therapeutic target which enhance the anti-tumor effects of radiotherapy in NSCLC.

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Y Chromosome LncRNA Are Involved in Radiation Response of Male Non–Small Cell Lung Cancer Cells

Cited by 29 publications

References 54 publications

LncRNA FGD5-AS1 Facilitates the Radioresistance of Breast Cancer Cells by Enhancing MACC1 Expression Through Competitively Sponging miR-497-5p

LncRNA FGD5-AS1 Facilitates the Radioresistance of Breast Cancer Cells by Enhancing MACC1 Expression Through Competitively Sponging miR-497-5p

Long noncoding RNA LINC00958 suppresses apoptosis and radiosensitivity of colorectal cancer through targeting miR-422a

Silencing of lncRNA H19 Enhances the Sensitivity to X-rays and Carbon-Ions Through the miR-130a-3p /WNK3 Signal Axis in Non-Small-Cell Lung Cancer Cells

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