miRNA‑328 overexpression confers cisplatin resistance in non‑small cell lung cancer via targeting of PTEN

Wang, Chunmei; Wang, Shijun; Ma, Feng'e; Zhang, Wei-Dan

doi:10.3892/mmr.2018.9478

Cited by 17 publications

(18 citation statements)

References 27 publications

(25 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…More importantly, PTEN is also involved in drug resistance in NSCLC. For instance, aberrant expression of miR-328 causes cisplatin resistance by targeting PTEN in NSCLC [36]. miR-181 mediates cisplatin resistance in NSCLC through the PTEN/PI3 K/AKT pathway [37].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Involvement of miR-4262 in paclitaxel resistance through the regulation of PTEN in non-small cell lung cancer

et al. 2019

View full text Add to dashboard Cite

Non-small cell lung cancer (NSCLC) is considered to be the primary cause of cancer-related mortalities worldwide. Paclitaxel (PTX), either as a monotherapy or in combination with other drugs, is an alternative therapy for advanced NSCLC. However, cancer cell resistance against PTX represents a major clinical problem. This study aimed to investigate the role and underlying mechanism of miR-4262 in PTX-resistant NSCLC. The levels of miR-4262 were analysed by quantitative reverse transcription polymerase chain reaction. A luciferase reporter assay and bioinformatics were used to explore the potential target gene of miR-4262. Regulation of miR-4262 and PTEN expressions in NSCLC was conducted by transfection. PTX-resistant A549 and H1299 cells were established by stepwise screening through increasing the PTX concentration in the cultures. In vivo , tumorigenesis experiments were used to explore the effects of miR-4262 and PTX. Cell proliferation, apoptosis and cell migration were detected using a CCK-8 assay, flow cytometry and Transwell migration assay, respectively. PI3 K/Akt pathway-related proteins were detected by western blot. miR-4262 expression was significantly upregulated in NSCLC tissues and cell lines, and miR-4262 targeted PTEN. In addition, miR-4262 induced PTX chemoresistance by promoting survival and migration in A549/PTX and H1299/PTX cells. Moreover, miR-4262 expression and PI3 K/Akt signalling pathway-related proteins were upregulated and PTEN was downregulated in A549/PTX and H1299/PTX. Our results indicate that miR-4262 enhances PTX resistance in NSCLC cells through targeting PTEN and activating the PI3 K/Akt signalling pathway. The inhibition of miR-4262 expression might be an improved treatment to overcome PTX resistance in NSCLC.

show abstract

Section: Discussionmentioning

confidence: 99%

RETRACTED: Involvement of miR-4262 in paclitaxel resistance through the regulation of PTEN in non-small cell lung cancer

et al. 2019

View full text Add to dashboard Cite

show abstract

“…In the present study, miR-328-5p was determined to be overexpressed in NSCLC tumors. This is consistent with the RT-qPCR data from a previous study of NSCLC tumors (48). Similar to the effect in NSCLC cells transfected with TPTEP1, knockdown of miR-328-5p inhibited cell proliferation and induced cell apoptosis in NSCLC cells.…”

Section: Discussionsupporting

confidence: 91%

lncRNA TPTEP1 competitively sponges miR‑328‑5p to inhibit the proliferation of non‑small cell lung cancer cells

Cao

Wang²,

Feng

et al. 2020

Oncol Rep

View full text Add to dashboard Cite

Accumulating evidence suggests that lncRNAs are involved in almost all normal physiological processes and that aberrant expression of lncRNAs may be involved in the development of diseases, including non-small cell lung cancer (NSCLC). However, the roles of lncRNA-TPTE pseudogene 1 (TPTEP1) in lung cancer and the underlying molecular mechanisms have remained elusive. In the present study, significant downregulation of TPTEP1 in tumors compared with normal tissues from patients with NSCLC was observed. Overexpression of TPTEP1 inhibited cell proliferation and induced apoptosis in NSCLC cells. A bioinformatics analysis based on miRDB predicted microRNA (miR)-328-5p as a potential binding miRNA for TPTEP1. Using a dual-luciferase reporter assay and western blot analysis, it was further validated that TPTEP1 sponged miR-328-5p to upregulate Src kinase signaling inhibitor 1 (SRCIN1) in NSCLC cells. Through regulation of SRCIN1, TPTEP1 was indicated to inactivate the Src and STAT3 pathways in NSCLC cells. Notably, silencing of SRCIN1 reversed the TPTEP1 overexpression-induced inhibition of cell proliferation and increase of the apoptotic rate in NSCLC cells. Pearson correlation analysis revealed a significant positive correlation between TPTEP1 and SRCIN1 mRNA levels in NSCLC tumors. The present results provided insight into the roles of TPTEP1 in NSCLC and the underlying mechanisms.

show abstract

“…42 Previous studies also identified the involvement of miR-608 and miR-328 in the development of cisplatin resistance in NSCLC. 43,44 Furthermore, some circular RNAs, such as hsa_circ_0085131, circ_0076305 and hsa_circ_0001946, have been linked with the resistance to cisplatin in NSCLC. 8,45,46 These findings urge the attempt to investigate the role of lncRNAs in cisplatin resistance in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

<p>LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma</p>

Wang¹,

Gao²,

Chen³

et al. 2020

OTT

View full text Add to dashboard Cite

Background: Long non-coding RNAs (lncRNAs) have been found to contribute to cisplatin resistance in several cancers; however, the role of lncRNA LINC01116 in cisplatin resistance remains unknown in non-small-cell lung cancer. This study aimed to examine the contribution of LINC01116 to cisplatin resistance in lung adenocarcinoma (LAD). Materials and Methods: Cisplatin-resistant A549/DDP cells were generated by treatment with cisplatin by dose escalation. LINC01116 expression was compared between A549 and A549/DDP cells, and between cisplatin-resistant and non-resistant LAD specimens. The cell viability, colony formation, proliferation, migration and invasion were measured using MTT and Transwell assays, and cell apoptosis and cell cycle were detected using flow cytometry. The expression of E-cadherin and Vimentin was quantified. LAD xenografts were modeled in nude mice to investigate the role of LINC01116 on the resistance of LAD to cisplatin. Results: MTT assay measured the IC 50 values of 13.49 ± 1.62 and 3.52 ± 1.33 μg/mL for A549/DDP and A549 cells, respectively. LINC01116 was overexpressed in cisplatin-resistant LAD specimens and A549/DDP cells (P < 0.05). Knockdown of LINC01116 inhibited cell viability, proliferation, migration and invasion, promoted apoptosis and enhanced the sensitivity to cisplatin in A549/DDP cells, while LINC01116 overexpression promoted cell viability, proliferation, migration and invasion, inhibited apoptosis and reduced the sensitivity to cisplatin in A549 cells. LINC01116 knockdown resulted in a 2.1-fold increase in E-cadherin expression and a 56% reduction in Vimentin expression in A549/DDP cells, and LINC01116 overexpression resulted in a 45% reduction in E-cadherin expression and a 1.82fold increase in Vimentin expression in A549 cells. Conclusion: Dysregulation of lncRNA LINC01116 expression results in resistance of LAD to cisplatin via the EMT process. Our findings support the oncogenic role of LINC01116 to promote the development of cisplatin resistance in LAD, and LINC01116 may be a novel predictor of poor response to cisplatin.

show abstract

miRNA‑328 overexpression confers cisplatin resistance in non‑small cell lung cancer via targeting of PTEN

Cited by 17 publications

References 27 publications

RETRACTED: Involvement of miR-4262 in paclitaxel resistance through the regulation of PTEN in non-small cell lung cancer

RETRACTED: Involvement of miR-4262 in paclitaxel resistance through the regulation of PTEN in non-small cell lung cancer

lncRNA TPTEP1 competitively sponges miR‑328‑5p to inhibit the proliferation of non‑small cell lung cancer cells

<p>LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma</p>

Contact Info

Product

Resources

About