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Published on: August 23, 2024
SNHG7 mediates cisplatin-resistance in non-small cell lung cancer by activating PI3K/AKT pathway
K Chen1, A Abuduwufuer, H Zhang
1Department of Thoracic, Xinjiang Uygur Autonomous Region People's Hospital, Urumqi, China. imic6000@sina.com.
Objective:
The aim of this study was to clarify the function of long noncoding ribonucleic acids (lncRNAs) small nucleolar RNA host gene 7 (SNHG7) in cisplatin-resistant non-small cell lung cancer (NSCLC), and to explore the potential mechanism.
Patients And Methods:
SNHG7 expression in NSCLC and para-cancerous tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Meanwhile, the correlation between SNHG7 expression with clinical stage and cisplatin-resistance in NSCLC patients was analyzed. After transfection of si-SNHG7 or p-complementary deoxyribonucleic acid (pcDNA)-SNHG7, changes in cellular behaviors of A549/DDP cells were evaluated, including cell viability, apoptosis, migration, invasion and cell cycle. The regulatory effects of SNHG7 on the expressions of genes were determined by qRT-PCR as well. Furthermore, Western blot was conducted to determine the protein expressions of drug-resistance genes minimal residual disease1 (MRD1), P-glycoprotein (P-gp), BCRP and relative genes in phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway.
Results:
Compared with adjacent normal tissues, SNHG7 was highly expressed in NSCLC tissues. Moreover, SNHG7 expression was significantly higher in advanced-stage NSCLC patients than those in early-stage. SNHG7 level remained significantly higher in DDP-resistant NSCLC tissues and cell lines as well. Knockdown of SNHG7 remarkably enhanced cisplatin-resistance in NSCLC cells, manifesting as decreased cell viability, migratory and invasive rates, DNA synthesis capacity, and promoted apoptosis. Meanwhile, SNHG7 knockdown down-regulated the mRNA levels of matrix metalloprotein2 (MMP2), MMP7 and MMP9 in vitro. After SNHG7 knockdown, the expressions of drug-resistant and relative genes in the PI3K/AKT pathway were notably down-regulated.
Conclusions:
SNHG7 induces the development of cisplatin-resistance in NSCLC through upregulating MRD1 and BCRP via PI3K/AKT pathway.
Insights
Small nucleolar RNA host gene 7 (SNHG7) is highly expressed in cisplatin-resistant non-small cell lung cancer (NSCLC). Upregulating minimal residual disease 1 (MRD1) and BCRP via the PI3K/AKT pathway, SNHG7 promotes drug resistance.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality worldwide.
- Cisplatin resistance is a major challenge in NSCLC treatment, necessitating the identification of novel therapeutic targets.
- Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in cancer progression and drug resistance.
Purpose of the Study:
- To investigate the functional role of the lncRNA small nucleolar RNA host gene 7 (SNHG7) in cisplatin-resistant NSCLC.
- To elucidate the underlying molecular mechanisms by which SNHG7 influences cisplatin resistance in NSCLC.
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess SNHG7 expression in NSCLC tissues and cell lines.
- Cellular assays evaluated the impact of SNHG7 modulation on cell viability, apoptosis, migration, invasion, and cell cycle progression.
- Western blot analysis was performed to examine the protein expression of drug resistance markers and key signaling pathway components.
Main Results:
- SNHG7 expression was significantly upregulated in NSCLC tissues compared to adjacent normal tissues, and higher in advanced-stage and cisplatin-resistant cases.
- Knockdown of SNHG7 in NSCLC cells enhanced cisplatin sensitivity, reducing cell viability and invasion while promoting apoptosis.
- SNHG7 modulated the expression of matrix metalloproteinases (MMPs) and key genes in the PI3K/AKT pathway, including MRD1 and BCRP.
Conclusions:
- SNHG7 plays a crucial role in the development of cisplatin resistance in NSCLC.
- The mechanism involves the upregulation of drug resistance genes, specifically minimal residual disease 1 (MRD1) and BCRP, mediated by the PI3K/AKT signaling pathway.
- Targeting SNHG7 may represent a potential therapeutic strategy to overcome cisplatin resistance in NSCLC.
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