
==== Front
J Cardiothorac Surg
J Cardiothorac Surg
Journal of Cardiothoracic Surgery
1749-8090
BioMed Central London

39300525
3048
10.1186/s13019-024-03048-4
Research
Detection of serum SNHG22 and its correlation with prognosis of non-small cell lung cancer
Cheng Quan 1
Chen Guoping 2
Wu Xiaojiao YKwuxiaojiao1986@163.com

3
Fang Hang 3
Shi Jingjing 3
Zhong Bonian zhongbonian01@163.com

4
1 grid.494629.4 0000 0004 8008 9315 Department of Traditional Chinese Medicine, Affiliated Hangzhou First People’s Hospital, School of Medicine, Westlake University, Hangzhou, 310006 China
2 https://ror.org/030a08k25 Department of Respiratory and Critical Care Medicine, Binhai County People’s Hospital, Yancheng, 224500 China
3 Department of Laboratory, The First People’s Hospital of Yongkang, No. 52, Lizhou North Road, Yongkang, 321300 China
4 grid.410737.6 0000 0000 8653 1072 Department of Pulmonary and Critical Care Medicine, The Fourth Affiliated Hospital of Guangzhou Medical University, No.1, Guangming East Road, Guangzhou, 511300 China
20 9 2024
20 9 2024
2024
19 53616 5 2024
9 9 2024
© The Author(s) 2024
2024
https://creativecommons.org/licenses/by-nc-nd/4.0/ Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.
Background

Lung cancer accounts for a significant proportion of cancer-related deaths in China, with the majority of the cases being classified as non-small cell lung cancer (NSCLC). The study aimed to investigate the expression of serum SNHG22 in patients with NSCLC, and its molecular mechanism and prognostic potential in NSCLC.

Methods

Admitted 125 NSCLC patients were selected for the study, along with 125 healthy individuals in the same period. The levels of SNHG22 and miR-128-3p were quantified via RT-qPCR. Correlations between the SNHG22 level and the pathological characteristics of the NSCLC patients were investigated through the application of the chi-square test. The targeting relationship between SNHG22 and miR-128-3p was predicted by online database and confirmed by luciferase activity. The prognostic ability of SNHG22 in NSCLC was assessed by Kaplan-Meier curves and multivariate Cox analysis.

Results

SNHG22 was upregulated in NSCLC and directly targeted miR-128-3p. The rate of overall survival is lower in patients with high-SNHG22 group compared to those with low-SNHG22 group. Silencing SNHG22 impaired the functionality of cells, which was restored by miR-128-3p inhibitor. SNHG22 stands as an independent predictor of poor prognosis in NSCLC patients.

Conclusion

The overexpression of SNHG22 in NSCLC is related to lymph node metastasis, TNM stage and patient survival, which is expected to be a prognostic predictor of NSCLC patients.

Keywords

Lung cancer
SNHG22
Prognosis
miR-128-3p
Biological function
Kangda College of Nanjing Medical University Research and Development Fund - Key ProjectNo. KD2023KYJJ028 issue-copyright-statement© BioMed Central Ltd., part of Springer Nature 2024
==== Body
pmcBackground

Lung cancer, a lethal disease, arises from the epithelial lining of the bronchial trees and is responsible for a significant number of cancer-related mortalities globally [1]. Statistically, lung cancer is diagnosed in approximately 1.8 million individuals globally each year, representing a prevalence rate of 13% [2]. NSCLC predominates as the prevalent form of lung cancer, comprising approximately 85% of lung cancer diagnoses [3]. Owing to the widespread presence of risk factors including tobacco exposure and air pollution, individuals with lung cancer in China encounter intense challenges in terms of treatment [4]. Meanwhile, NSCLC patients may exhibit no symptoms in the initial stages, and some are already experiencing metastasis by the time of diagnosis, which leads to unfavorable survival rates [5]. To elevate the survival of patients, it is crucial to refine the preventative strategies and the prognostic evaluations for lung cancer, thereby enhancing treatment efficacy and diminishing mortality among NSCLC patients.

Long non-coding RNAs (lncRNAs), which are non-coding RNAs exceeding 200 nucleotides in length, function within cells to modulate gene expression, affect protein activities, and contribute to the regulation of the cell cycle [6]. Progress has been made in the research of lncRNAs in the field of lung cancer, and these molecules are considered to have a significant impact on the onset, progression, and therapeutic responses of lung cancer [7, 8]. For example, lncRNA LINC00969 promotes tyrosine kinase inhibitor resistance in lung cancer by modulating NLRP3 and related pathways, thereby consequently impacts the progression of the disease [9]. LncRNA LINC00115 targets the miR-607/ITGB1 axis to mediate lung cancer progression and may be a candidate therapeutic target [10]. LncRNA PCAT1 was shown to mediate the cGAS/STING pathway to influence NSCLC genesis and immune response [11]. LncRNA SNHG22, an emerging lncRNA, is situated on chromosome 18q21.1, which is implicated in several diseases [12]. Wei and colleagues proposed that SNHG22 accelerates trophoblast growth by modulating the miR-128-3p/PCDH11X axis and maybe a potential marker for therapeutics in preeclampsia patients [13]. Yao et al. supported that the SNHG22/miR-128-3p/E2F3 regulatory network holds therapeutic promise of the colorectal cancer [14]. Furthermore, research has indicated that SNHG22 is implicated in the progression of osteosarcoma, esophageal cancer, and breast cancer [15–17]. However, little is known about the mechanism of action and potential application of SNHG22 in NSCLC.

Therefore, the aim of this study is to observe the level of SNHG22 in serum and cellular specimens, and explore its relationship with clinicopathological characteristics of NSCLC patients, with a view to providing more ideas to improve the prognosis of patients.

Methods

Inclusion of study subjects

Patients with NSCLC diagnosed and treated at The First People’s Hospital of Yongkang from September 2017 to February 2019 were the study subjects. The 125 NSCLC patients who participated in the study did not receive any antitumor treatment and were free of other diseases before sampling. Meanwhile, an equal number of volunteers who were examined in our hospital and were in good health were included as control samples. Patients with NSCLC were followed up by telephone or outpatient for 60 months after discharge to obtain survival information.

This study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the Ethics Committee of The First People’s Hospital of Yongkang. The aforementioned participants all volunteered to participate in this project after understanding the purpose of the study and written informed consent were provided from the participants involved.

Processing of serum samples

Blood samples obtained from NSCLC patients and healthy individuals were promptly centrifuged (3000 rpm, 15 min, 4 °C), and then stored in a -80 °C refrigerator for backup.

Culturing of NSCLC cells

Laboratory cultures of lung cancer cells (CAL12T, H273, H1703, and H23) and bronchial epithelial cells (BEAS2B) provided by ATCC (USA) were performed. The cells were separately cultured in DMEM medium (Thermo Fisher Scientific, USA) supplemented with 10% FBS (Hyclone, USA). The incubator was set at 37 °C and 5% CO2.

Transfection of cells

Lung cancer cells were transferred to 6-well plates for incubation, and si-NC, si-SNHG22, si-SNHG22 + inhibitor NC, and si-SNHG22 + miR-128-3p inhibitor were transfected by lipofectamine 3000 (Invitrogen, USA) reagent into CAL12T and H1703 cells. The above fragments were synthesized by Shanghai GenePharma (China).

RT-qPCR assay

Total RNA was extracted from serum and cell samples by TRIZOL kit (Takara, Japan). After the RNA concentration and purity were qualified, cDNA was synthesized by Reverse Transcription kit (Qiagen, Germany) and stored at 4 °C. A 20 µL reaction system was configured according to the SYBR Premix Ex Taq kit (Vazyme, Nanjing, China), and the PCR reaction was performed on 7500 Real-Time PCR system (Applied Biosystems, USA). SNHG22 and miR-128-3p were corrected with GAPDH and U6 as internal controls, respectively, and their levels were calculated using the 2−ΔΔCt method. The primer sequences are as follows: (forward) TAAGAGTGGCCTCTGCGTG, (reverse) AGGCACCTAACAGGGGAG for SNHG22; (forward) GGGAATCACAGTGAACCG, (reverse) CAGTGCGTGTCGTGGAGT for miR-128-3p; (forward) ACTCATGACCACAGTCCAT, (reverse) AGGCACCTAACAGGGGAG for GAPDH; (forward) CTCGCTTCGGCAGCACA, (reverse) CGCTTCACGAATTTGCGT for U6.

CCK-8 assay

CAL12T and H1703 cells were transferred to 96-well plates and the density was adjusted to 3 × 103 cells/well, and the CCK-8 reagent (Beyotime, China) was added to the well plates at specific time intervals. Following a 2-hour incubation period, the absorbance was measured. This process was repeated daily for three days.

Transwell assay

Cells at a density of 2 × 104 cells/well were introduced into the upper compartment of the transwell plate, with DMEM and FBS being positioned in the lower compartment beneath. The cells transferred to the lower part of the chamber after 24 h were stained and counted to calculate the level of cell migration. Alternatively, the level of cell invasion was measured following the same procedure as described above after coating the upper layer of transwell plates with Matrigel.

Luciferase reporter assay

The downstream targets of SNHG22 were predicted by ENCORI, DIANA Tools and LncBook 2.0 online databases, and the connection sites of SNHG22 and miR-128-3p were provided. Furthermore, SNHG22 wild-type and mutant-type (SNHG22-WT and SNHG22-MUT) fragments were generated by pmirGLO plasmid (Promega, USA). The above fragments were sequentially co-transfected with miR-128-3p mimic/inhibitor and mimic/inhibitor NC using lipofectamine 3000 into CAL12T cells incubated in 24-well plates. After 48 h of co-transfection, the luciferase activity of the cells was assayed by the Dual-Luciferase Activity kit (Promega, USA).

Statistical analysis

Count data were represented as n, and between groups were tested by independent t-test. The correlation between SNHG22 and miR-128-3p levels was analyzed by Pearson correlation analysis. The survival curve of NSCLC patients was drawn by Kaplan-Meier method with the Log-rank test. The effects of prognostic factors were identified using multivariate Cox proportional hazards model. P < 0. 05 indicated that the difference was statistically significant.

Results

Expression of SNHG22 in NSCLC

Serum SNHG22 expression was elevated in the NSCLC group compared to the healthy group (Fig. 1A), and the SNHG22 levels were all higher in lung cancer cells than in bronchial epithelial cells (Fig. 1B). SNHG22 was prominently expressed in CAL12T and H1703 cells and thus served as the study samples for in vitro cell assays.

Fig. 1 Serum SNHG22 expression and its prognostic significance in NSCLC. (A) SNHG22 was upregulated in the serum of NSCLC patients. (B) SNHG22 levels were obviously increased in lung cancer cells. (C) The prognostic survival of NSCLC patients in the low-SNHG22 group was better than that in the high-SNHG22 group (P = 0.020). ***P < 0.001

Association of differentially expressed SNHG22 with clinical indicators in NSCLC patients

Evaluation of clinical indicators revealed a high percentage of NSCLC patients with high serum SNHG22 expression who developed lymph node metastasis and were in advanced TNM stage, which means that upregulation of SNHG22 correlates with lymph node metastasis (P = 0.020) and TNM stage (P = 0.018) in patients (Table 1).

Table 1 Correlation between abnormal levels of SNHG22 and clinical parameters in non-small cell lung cancer patients

Parameters	Total
(n = 125)	SNHG22 level	P values	
High (n = 68)	Low (n = 57)	
Gender				0.671	
   Male	72	38	34	
   Female	53	30	23	
Age				0.794	
   ≤ 60 years	62	33	29	
   > 60 years	63	35	28	
Tumor size				0.078	
   ≤ 5 cm	66	31	35	
   > 5 cm	59	37	22	
Smoking				0.570	
   Yes	80	42	38	
   No	45	26	19	
Differentiation				0.227	
   Well-Moderate	60	36	24	
   Poor	65	32	33	
Lymph node metastasis				0.020	
   Negative	67	30	37	
   Positive	58	38	20	
TNM stage				0.018	
   I-II	58	25	33	
   III-IV	67	43	24	

Ability of SNHG22 in the prognosis of NSCLC patients

Figure 1C illustrates that the high SNHG22 expression group (n = 68) had a lower overall survival rate than the low expression group (n = 57) at 60 months (P = 0.020). Moreover, Cox analysis confirmed that SNHG22 (P = 0.008), lymph node metastasis (P = 0.031) and TNM stage (P = 0.040) were risk indicators for the prognosis of NSCLC patients (Table 2).

Table 2 Multivariate Cox analysis of clinical indicators associated with overall survival in patients with non-small cell lung cancer

Indicators	HR	95% CI	P	
SNHG22	0.198	0.060–0.653	0.008	
Gender	0.727	0.306–1.725	0.469	
Age	0.644	0.238–1.745	0.387	
Tumor size	0.422	0.167–1.063	0.067	
Smoking	1.587	0.665–3.788	0.298	
Differentiation	0.296	0.068–1.293	0.106	
Lymph node metastasis	0.239	0.065–0.877	0.031	
TNM stage	2.510	1.042–6.045	0.040	

Level of mir-128-3p in NSCLC

Bioinformatics websites predicted the downstream targets of SNHG22 and drew the related Venn diagram (Fig. 2A), and there were complementary sequences between SNHG22-WT and miR-128-3p (Fig. 2B). The luciferase activity of CAL12T cells was reduced after co-transfection with SNHG22-WT and miR-128-3p mimic, while enhanced after co-transfection with SNHG22-WT and miR-128-3p inhibitor. In addition, transfection of SNHG22-MUT did not produce significant regulation of luciferase activity (Fig. 2C), implicating miR-128-3p as a downstream target of SNHG22. miR-128-3p was verified to be lowly expressed in NSCLC serum (Fig. 2D) and cells (Fig. 2E). NSCLC patients’ serum SNHG22 was negatively correlated with miR-128-3p expression by Pearson’s analysis (Fig. 2F, r = -0.662, P < 0.001).

Fig. 2 SNHG22 directly targets miR-128-3p. (A) Venn diagram of SNHG22 downstream target prediction. (B) Complementary sequences exist for SNHG22 and miR-128-3p. (C) Luciferase activity assay of CAL12T cells. (D) Serum miR-128-3p was reduced in the NSCLC group. (E) miR-128-3p levels were downregulated in lung cancer cells. (F) Linear scatter plot of serum SNHG22 and miR-128-3p expression (r = -0.662, P < 0.001). *P < 0.05, ***P < 0.001

Effect of dysregulation of SNHG22 and mir-128-3p on cell activity

Upon transfection of si-SNHG22 in CAL12T and H1703 cells, miR-128-3p levels were significantly upregulated, and the prominent expression was counteracted by co-transfection of miR-128-3p inhibitor (Fig. 3A). Knockdown of SNHG22 inhibited the growth of lung cancer cells, while si-SNHG22 + miR-128-3p inhibitor promoted the cell viability (Fig. 3B). Meanwhile, when SNHG22 levels were decreased, the migration and invasion of lung cancer cells were also suppressed, and the intervention of miR-128-3p inhibitor counteracted this inhibitory effect (Fig. 3C and D).

Fig. 3 Regulation of CAL12T and H1703 cell activity by silencing SNHG22 and miR-128-3p. (A) Knockdown of SNHG22 increased miR-128-3p in lung cancer cells, while co-transfection of miR-128-3p inhibitor restored the level of miR-128-3p. (B-D) Dysregulation of SNHG22 had a repressive effect on the biological functions of lung cancer cells, which was reversed by the si-SNHG22 + miR-128-3p inhibitor. 200× magnification; **P < 0.01, ***P < 0.001, vs. control; #P < 0.05, ###P < 0.001, vs. si-SNHG22

Discussion

In the past few years, the detection rate of NSCLC has been improved with the improvement of residents’ health awareness and the deepening of clinical research [18]. Meanwhile, based on the improvement of the level of surgery and the wide application of targeted agents, the survival period of NSCLC patients has been prolonged to a great extent [19]. Nonetheless, the outcomes for some patients with NSCLC still cannot meet the desired clinical goals, and there is still room for improvement. Therefore, screening factors associated with the prognosis of NSCLC patients and identifying highly sensitive biological indicators to predict the prognostic outcomes of patients have positive research value in enhancing clinical interventions for NSCLC patients and improving their prognostic survival.

LncRNAs are an emerging class of epigenetic regulatory molecules that participate in various physiological processes of an organism by interfacing with microRNAs (miRNAs) [20]. Earlier studies demonstrated that lncRNA LINC02159, DUXAP8 and HOXC-AS3 were all enriched in NSCLC [21–23]. The results of this study showed that serum SNHG22 was actively expressed in NSCLC and was associated with poor survival of patients. Moreover, overexpression of SNHG22 was linked to lymph node metastasis and the TNM staging of patients, suggesting its involvement in the progression of NSCLC. Additionally, SNHG22 was demonstrated to be a prognostic risk indicator for NSCLC using multifactorial COX analysis, implying that SNHG22 may be used for the prediction of prognostic outcomes in NSCLC patients with good efficacy.

miRNAs were stated to be implicated in the pathogenesis of NSCLC [24]. miR-128-3p exhibits altered expression in tumors, and modifications in its levels are commonly related to the initiation, progression, and prognosis of tumors. According to the study from Yang and her colleagues, FOXD3‑AS1 bound to miR‑128‑3p to enhance the levels of LIMK1, thereby speeding up the progression of cervical cancer [25]. More importantly, miR-128-3p is thought to have decreased levels in NSCLC [26, 27], consistent with our assay results. In this study, miR-128-3p was confirmed as a downstream target of SNHG22 by on-line evaluation and luciferase activity assay. miR-128-3p level was decreased in NSCLC serum and cells, which was negatively regulated by SNHG22, indicating that SNHG22 mediates NSCLC progression through sponge miR-128-3p. Furthermore, SNHG22 silencing and miR-128-3p inhibitor were transfected into NSCLC cells. In vitro cellular experiments revealed that the growth cycle and metastatic ability of NSCLC cells were suppressed when SNHG22 was knocked down. Our results are further supported by evidence that SNHG22 was prominently expressed in gastric cancer, and downregulation of SNHG22 impeded the growth and accelerated the apoptosis of gastric cancer cell [28]. Meanwhile, the negative effects of low-expressed SNHG22 on NSCLC cells were restored after co-transfection of miR-128-3p downregulation and silencing of SNHG22, confirming the direct targeting ability of SNHG22 to miR-128-3p.

Interestingly, Xie et al. recognized that NEAT1/miR-128-3p binding to ADAM28 affected apoptosis in NSCLC cells [27]. In addition, miR-128-3p negatively regulated downstream MSTO2P to mediate lung cancer cell viability as noted by Gu and his colleagues [29]. Based on this, we will further refine the regulatory network of SNHG22/miR-128-3p axis in NSCLC in subsequent work. The establishment of animal models will also contribute to the further validation of the prognostic value of SNHG22 in NSCLC. Moreover, the related research about SNHG22 clinical inhibitor can also help us to broaden the research direction.

Conclusions

In summary, SNHG22 expression was elevated and miR-128-3p level was decreased in serum and cells of NSCLC patients. The upregulation of SNHG22 is closely related to lymph node metastasis, TNM stage and poor prognosis of patients. The biological activity of cells decreased after SNHG22 levels were suppressed, which was repaired by the intervention of miR-128-3p inhibitor. SNHG22 was proposed to predict the prognostic outcome of NSCLC patients, potentially serving as an adjunctive bioindicator of NSCLC prognosis.

Acknowledgements

Not applicable.

Author contributions

Q C and GP C contributed to the study conception and design. Material preparation and data collection were performed by XJ W, H F and JJ S. Data analysis was conducted by XJ W and BN Z. The first draft of the manuscript was written by Q C and GP C and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

Funding

The study was supported by Kangda College of Nanjing Medical University Research and Development Fund - Key Project (No. KD2023KYJJ028).

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

This study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the Ethics Committee of The First People’s Hospital of Yongkang. The aforementioned participants all volunteered to participate in this project after understanding the purpose of the study and informed consent has been obtained from the participants involved.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.

Abbreviations

lncRNAs Long non-coding RNAs

miRNAs microRNAs

NSCLC Non-small cell lung cancer

Publisher’s note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Quan Cheng and Guoping Chen contributed equally to this work.
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