&lt;p&gt;FGFR1 Induces Acquired Resistance Against Gefitinib By Activating AKT/mTOR Pathway In NSCLC&lt;/p&gt;

Zhang, Dan; Han, Lili; Du, Fei; Liu, Xiaomeng; Jin, Li; Song, Minghui; Zeng, Li; Li, Guo-yin

doi:10.2147/ott.s220462

Cited by 15 publications

(22 citation statements)

References 31 publications

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“…A recent study reported that HAX1 prevents glioblastoma cells from apoptosis through the Akt1 pathway, 15 and it has also been reported that the AKT/mTOR signal pathway plays an important role in NSCLC. AKT/mTOR signal pathway induces gefitinib‐resistant of NSCLC 19 . FAM83D has been reported to improve epithelial‐mesenchymal transition, invasion and cisplatin resistance through activating the AKT/mTOR pathway in NSCLC 20 .…”

Section: Resultsmentioning

confidence: 99%

“…AKT/mTOR signal pathway induces gefitinib-resistant of NSCLC. 19 FAM83D has been reported to improve epithelialmesenchymal transition, invasion and cisplatin resistance through activating the AKT/mTOR pathway in NSCLC. 20 The oncogene IARS2 promotes the occurrence of NSCLC by activating the AKT/MTOR pathway.…”

Section: Silencing Of Hax1 Reduces Invasion and Epithelial-mesenchymamentioning

confidence: 99%

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HAX1 enhances the survival and metastasis of non‐small cell lung cancer through the AKT/mTOR and MDM2/p53 signaling pathway

et al. 2020

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Background HS‐1‐associated protein‐1 (HAX1) has been reported to be overexpressed in non‐small cell lung cancer (NSCLC) tissues. However, the underlying mechanism of HAX1 in NSCLC has not previously been demonstrated. The present study investigated the role and underlying mechanism of HAX1 in NSCLC. Methods The HAX1 expression were confirmed in NSCLC tissues through TCGA database and qRT‐PCR. Moreover, we performed qRT‐PCR, Western blotting, Transwell assays, TUNEL assays and so on to evaluate the role of HAX1 in A549 and H1299 cell lines. Results mRNA expression of HAX1 was overexpressed in NSCLC tissues compared to adjacent normal tissues according to The Cancer Genome Atlas (TCGA) database. QRT‐PCR assays showed that HAX1 mRNA expression was upregulated in NSCLC tissues. The high HAX1 mRNA levels were found to be positively associated with tumor size, TNM stage and lymphatic metastasis. Silencing of HAX1 promoted apoptosis and reduced invasion of A549 and H1299 cells by inhibiting the AKT/mTOR and MDM2/P53 signal pathway. AKT agonist SC79 could inhibit apoptosis and promote proliferation, migration and invasion of A549 and H1299 cells transfected with si‐HAX1. Conclusions The present study provided a better understanding of HAX1 mechanism in NSCLC and potential therapeutic target for NSCLC.

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Section: Resultsmentioning

confidence: 99%

Section: Silencing Of Hax1 Reduces Invasion and Epithelial-mesenchymamentioning

confidence: 99%

HAX1 enhances the survival and metastasis of non‐small cell lung cancer through the AKT/mTOR and MDM2/p53 signaling pathway

et al. 2020

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“… 17 Besides, the expression of FGFR1 in NSCLC is significantly increased and high expression of FGFR1 implies an unfavorable prognosis of NSCLC patients; knockdown of FGFR1 sensitizes PC9 cells to gefitinib. 18 FGFR1 is proved to activate ERK signaling pathway, thereupon up-regulating expression of SOX2 and promoting the proliferation and migration of NSCLC cells. 19 Unfortunately, although the role of FGFR1 in NSCLC progression is confirmed and its inhibitors are designed to treat NSCLC, most of the studies are still at preclinical stage and the application of FGFR1 inhibitors in the clinical treatment of NSCLC is still facing great challenges.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

LncRNA PVT1 Facilitates Proliferation, Migration and Invasion of NSCLC Cells via miR-551b/FGFR1 Axis

Wang¹,

Cheng²,

Dai³

et al. 2021

OTT

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Background Long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) plays a crucial role in non-small cell lung cancer (NSCLC). Nonetheless, regulatory effects of PVT1 on functions of NSCLC cells remain blurry. Methods Relative expression levels of PVT1, miR-551b and FGFR1 mRNA in tumor tissues and cells were examined employing quantitative real-time polymerase chain reaction (qRT-PCR); CCK-8 and BrdU assays were utilized for measuring cell viability and proliferation of H1299 and A549 cells; cell migration and invasion were detected deploying Transwell assay; dual-luciferase assay was used for the validation of binding sequence between PVT1 and miR-551b. FGFR1 expression in protein level was quantified employing Western blot. Results PVT1 was highly expressed in NSCLC tissues and cell lines, whereas miR-551b expression was down-regulated. Overexpression of PVT1 potentiated viability, proliferation, migration and invasion of NSCLC cells while miR-551b inhibited the biological behaviors mentioned above. MiR-551b was predicted and then confirmed as a direct downstream target of PVT1. Meanwhile, a negative correlation was observed between PVT1 expression and miR-551b expression in NSCLC tissues. Besides, PVT1 could increase FGFR1 expression by repressing miR-551b expression. Conclusion PVT1 promotes the proliferation, migration and invasion of NSCLC cells by indirectly mediating FGFR1 via targeting miR-551b.

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“…The H-score system was used to assess the expression of target proteins, and the formula for the H-score is as follows: Histoscore = Σ (I × Pi), where I = intensity of staining and Pi = percentage of stained tumor cells [28]. MDA-MB-231 cells were seed on the dish with a density of about 30% and treated with 400 nM Mith A for 24 h. Immuno uorescence (ICC) was performed as described in our previous study [29].…”

Section: Transwell Migration Assaymentioning

confidence: 99%

E3 Ubiquitin Ligase NEDD4L Negatively Regulates Breast Cancer Metastasis By Downregulating SNAI2

Zuo¹,

Li²,

Li³

et al. 2021

Preprint

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Background Accumulating evidence demonstrated that the abnormal expression of E3-ubiquitin ligase NEDD4L plays an important role in the biological process of carcinomas. However, its role in breast cancer (BRCA) remains elusive. Methods The expression of NEDD4L was analyzed using BRCA datasets from public database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were used for enrichment analysis. Both transwell assay and pulmonary metastasis model of BRCA were used to detect metastatic ability of cells. Western blotting, immunohistochemistry and immunofluorescence assay were used to detect the protein expression of target genes. The riskScore and nomogram were used to evaluate the prognosis of patients. Results NEDD4L was significantly downregulated in cancer tissues and positively correlated with the overall survival of patients. Knocking down NEDD4L could enhance the migration and metastasis ability of BRCA cells. SP1 promotes NEDD4L expression, resulting in SNAI2 downregulation in BRCA. A NEDD4L related to the prognostic model developed by LASSO Cox regression could be an independent predictive factor for BRCA. A nomogram combining riskScore and clinical indicators was established to evaluate the prognosis of BRCA quantitatively. Conclusions This study first reveals the role of the SP1/NEDD4L/SNAI2 axis in BRCA and establishes a reliable prognostic model, which provides a novel target and basis for clinical treatment and prognosis evaluation of breast cancer.

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<p>FGFR1 Induces Acquired Resistance Against Gefitinib By Activating AKT/mTOR Pathway In NSCLC</p>

Cited by 15 publications

References 31 publications

HAX1 enhances the survival and metastasis of non‐small cell lung cancer through the AKT/mTOR and MDM2/p53 signaling pathway

HAX1 enhances the survival and metastasis of non‐small cell lung cancer through the AKT/mTOR and MDM2/p53 signaling pathway

LncRNA PVT1 Facilitates Proliferation, Migration and Invasion of NSCLC Cells via miR-551b/FGFR1 Axis

E3 Ubiquitin Ligase NEDD4L Negatively Regulates Breast Cancer Metastasis By Downregulating SNAI2

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