CN115873955B - Kit for evaluating sensitivity of cisplatin to lung adenocarcinoma - Google Patents
Kit for evaluating sensitivity of cisplatin to lung adenocarcinoma Download PDFInfo
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- CN115873955B CN115873955B CN202211664856.XA CN202211664856A CN115873955B CN 115873955 B CN115873955 B CN 115873955B CN 202211664856 A CN202211664856 A CN 202211664856A CN 115873955 B CN115873955 B CN 115873955B
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- 208000010507 Adenocarcinoma of Lung Diseases 0.000 title claims abstract description 39
- 201000005249 lung adenocarcinoma Diseases 0.000 title claims abstract description 39
- 230000035945 sensitivity Effects 0.000 title claims abstract description 19
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- 239000003153 chemical reaction reagent Substances 0.000 claims abstract description 5
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- TXJZRSRTYPUYRW-NQIIRXRSSA-N methyl (1s,3r)-2-(2-chloroacetyl)-1-(4-methoxycarbonylphenyl)-1,3,4,9-tetrahydropyrido[3,4-b]indole-3-carboxylate Chemical compound C1([C@H]2C3=C(C4=CC=CC=C4N3)C[C@@H](N2C(=O)CCl)C(=O)OC)=CC=C(C(=O)OC)C=C1 TXJZRSRTYPUYRW-NQIIRXRSSA-N 0.000 description 11
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Abstract
The invention discloses a kit for evaluating sensitivity of cisplatin to lung adenocarcinoma. The invention is based on a series of cell experiments, and the result shows that the gene RETSAT has important mediating effect on iron death, so that RETSAT is inferred to be suitable for judging the sensitivity of lung adenocarcinoma patients to cisplatin treatment as a prognostic index. Then, the qPCR method is adopted to detect the RETSAT expression condition in the surgical excision specimens of 34 patients receiving cisplatin treatment, and the prognosis condition is analyzed, so that the patients with RETSAT high expression are more sensitive to patients with lower expression of cisplatin treatment, and the prognosis is better. Therefore, the expression level RETSAT can be used for predicting whether a lung adenocarcinoma patient is sensitive or resistant to cisplatin treatment, the expression quantity of RETSAT can be conveniently detected by using the existing detection reagent, and the lung adenocarcinoma patient has good clinical application value and popularization and application value.
Description
Technical Field
The invention relates to a kit for evaluating sensitivity of cisplatin to lung adenocarcinoma, and belongs to the technical field of biomedicine.
Background
Lung cancer is the most common tumor with the highest mortality, and both morbidity and mortality rank the first of all tumors. Among them, lung adenocarcinoma is one of the most common subtypes. Cisplatin acts to kill tumor cells by forming adducts with tumor cell DNA, resulting in DNA damage. Cisplatin-based combination chemotherapy is a first-line treatment regimen for lung adenocarcinoma, but a significant proportion of patients cannot benefit from it because of drug resistance issues. Therefore, a series of reliable biomarkers are needed to assist clinicians in predicting the sensitivity of lung adenocarcinoma patients to cisplatin chemotherapy, which is of great significance for improving the therapeutic effect of patients.
Some possible biomarkers (such as thymidylate synthase and the like) are reported to be used for predicting the sensitivity of lung adenocarcinoma patients to cisplatin combined chemotherapy, but the biomarkers cannot be widely used in clinic due to high cost, complicated process, low accuracy and the like, and the markers with higher sensitivity, specificity and application value can still be applied to the establishment of individual chemotherapy schemes of lung adenocarcinoma patients.
Iron death (Ferroptosis) was first proposed by dr.brunt r.stock well, university of columbia in 2012, and is a novel programmed death pattern distinct from apoptosis, cell necrosis, and cell coke death. The main mechanism is that external stimulus induces imbalance of reactive oxygen species (Reactive oxygen species, ROS) in cells, so that in Fenton reaction catalyzed by ferrous iron, polyunsaturated fatty acid (Poly-unsaturated FATTY ACID, PUFA) on a biological membrane is peroxidized, thereby causing phospholipid bilayer structure change, cell membrane rupture and finally cell death. Iron death, an important cell death mode, is involved in a range of pathophysiological processes. Therefore, iron death has received extensive attention from researchers in recent years, and research has been made into the mechanism of iron death and its application in diagnosis and treatment of diseases. Particularly in tumors, the prior research reports that chemotherapy can lead to iron death, and one research published earlier in the subject group shows that the iron death level of the tumors can be regulated by intervening in iron death related genes, so that the drug resistance phenomenon of the tumors to cisplatin chemotherapy is improved.
Disclosure of Invention
The purpose of the invention is that: aiming at the problems of the biomarker for evaluating the sensitivity degree of a lung adenocarcinoma patient to cisplatin chemotherapy at present, the invention provides a novel biomarker RETSAT (Retinol saturase, retinol saturated enzyme) for judging the sensitivity of the lung adenocarcinoma patient to tumor cell iron death caused by cisplatin chemotherapy, thereby evaluating the suitability of the patient for treating lung adenocarcinoma by using cisplatin.
In order to achieve the above purpose, the invention provides application of a reagent for detecting RETSAT expression quantity in preparing a kit for detecting and evaluating sensitivity of cisplatin to lung adenocarcinoma.
Preferably, the kit further comprises a specification, wherein the specification records an evaluation cut-off value of RETSAT expression quantity, the evaluation cut-off value is 8.809, and if RETSAT expression quantity DeltaCT in a detection sample is more than 8.089, the patient is tolerant to cisplatin chemotherapy; if RETSAT expression quantity DeltaCT in the detected sample is less than or equal to 8.089, the patient is resistant to cisplatin.
Preferably, the test sample is tumor tissue.
The invention also provides a kit for evaluating the sensitivity of cisplatin to lung adenocarcinoma, which at least comprises a reagent for specifically detecting RETSAT expression quantity.
The invention firstly adopts the whole genome CRISPR/Cas9 knockout screening technology, and is proved in the following cell experiments: knock-out RETSAT (fully designated Retinol Saturase, retinol saturated enzyme, ensembl: ENSG 00000042445.) significantly improved the tolerance of a549 lung adenocarcinoma cells to iron death inducer RSL 3. Considering that cisplatin also has the effect of causing iron death, RETSAT is knocked out or overexpressed in two lung adenocarcinoma cell lines of A549 and H358, and is treated by cisplatin, the drug resistance of cells to cisplatin is obviously improved after RETSAT is knocked out, and the killing capacity of cisplatin to lung adenocarcinoma cells is obviously improved after RETSAT is overexpressed. From this, RETSAT is inferred to be suitable as a prognostic indicator for determining the sensitivity of a lung adenocarcinoma patient to cisplatin treatment. Then, the qPCR method is adopted to detect the RETSAT expression condition in the surgical excision specimens of 34 patients receiving cisplatin treatment, and the prognosis condition is analyzed, so that the patients with RETSAT high expression are more sensitive to patients with lower expression of cisplatin treatment, and the prognosis is better. The expression level of RETSAT can thus be used to predict whether a patient with lung adenocarcinoma is susceptible to or resistant to cisplatin treatment.
Compared with the prior art, the invention has the beneficial effects that:
Based on a series of cell experiments and clinical data verification, the gene RETSAT (Retinol saturase, retinol saturated enzyme) has important mediating effect on iron death, and the expression level of the gene is closely related to the sensitivity of cells to an iron death inducer and cisplatin combined treatment, so that the gene can be used as a biomarker to assist in pre-judging the sensitivity of lung adenocarcinoma patients to cisplatin treatment, can conveniently detect the expression level of RETSAT by using the existing detection reagent, and has good clinical application value and popularization and application value; and overcomes the problems of high cost, complicated flow, low accuracy, low applicability and the like of the prior biomarker (such as thymidylate synthase and the like) for pre-judging the sensitivity of lung adenocarcinoma patients to cisplatin combined chemotherapy.
Drawings
FIG. 1 is a graph showing drug toxicity profiles of knocked-out or over-expressed RETSAT and control A549, H358 lung adenocarcinoma cells, respectively, against different concentrations of RSL3 or Cisplatin (CDDP);
FIG. 2 shows lipid peroxidation levels of knock-out or over-expression RETSAT and control A549, H358 lung adenocarcinoma cells treated with RSL3 or Cisplatin (CDDP), respectively;
FIG. 3 is a graph showing the predicted survival of RETSAT expression levels in lung adenocarcinoma tissues.
Detailed Description
In order to make the invention more comprehensible, preferred embodiments accompanied with figures are described in detail below.
Example 1
Crispr/Cas9 whole genome high-throughput drug resistance gene screening:
Firstly, constructing a series of sgrnas according to the existing Crispr/Cas9 knockout library, transfecting the sgrnas into lung adenocarcinoma cells A549, ensuring that each cell is only transferred into one sgRNA or is not transferred into the sgrnas by adopting a proper virus dosage, and then killing the cells which are not transferred into the sgrnas by using puromycin treatment. Each of the A549 cells thus obtained had a random gene knocked out. Subsequently, treatment screening of knocked-out cells with iron death inducer RSL3 inhibited or even killed sensitive cells, while normal proliferation of drug resistant cells was unaffected. By high throughput sequencing analysis of sgrnas in pre-and post-treatment cells, respectively, changes in cellular activity following knock-out of each gene can be inferred. As a result of this step, RETSAT knockdown cell subsets were found to be significantly reduced after RSL3 treatment compared to the control. Experimental data are shown in table 1:
TABLE 1
| Gene | Log(Fc)RSL3 | Log(Fc)DMSO | Log(Fc)RSL3–Log(Fc)DMSO |
| RETSAT | 2.189 | 0.141 | 2.048 |
Here, log (Fc) RSL3 represents a logarithmic value of a fold change in expression value of a certain sgRNA after 3 days of RSL3 treatment of cells and before drug administration, and Log (Fc) DMSO represents a control group, i.e., a logarithmic value of a change in expression value of the same sgRNA after 3 days of DMSO treatment and before drug administration. From this, it can be inferred that lung adenocarcinoma cells were enhanced in their ability to tolerate RSL3 after RETSAT knockdown.
Example 2
Changes to RSL3 and cisplatin resistance following lung adenocarcinoma cell knockout or overexpression RETSAT:
The cells transfected by the lung adenocarcinoma cells A549 and H358 are respectively knocked out or over-expressed RETSAT and corresponding controls, then are respectively treated by RSL3 and cisplatin, and after the drug effect is exerted, the activity of the cells is detected by using CCK 8. As a result, cells knocked out RETSAT were found to have significantly higher tolerance to RSL3 and cisplatin than the control group, while overexpression RETSAT resulted in increased sensitivity of the cells to both drugs (fig. 1). Meanwhile, BODIPY lipid peroxidation experiments showed that cisplatin treatment significantly increased lung adenocarcinoma cell lipid peroxidation levels, suggesting that cisplatin resulted in iron death, while knock-out RETSAT significantly alleviated this effect (fig. 2). From this, it can be inferred that knockout RETSAT significantly enhanced the ability of lung adenocarcinoma cells to tolerate cisplatin-induced iron death.
Example 3
RETSAT expression in tumor tissue of lung adenocarcinoma patients receiving cisplatin chemotherapy and prognosis analysis of patients:
By adopting a qRT-PCR mode, the expression condition of RETSAT in tumor tissues of 34 lung adenocarcinoma patients receiving cisplatin combined chemotherapy is detected. Patients were then followed for up to 5 years or more, and the association of this miRNA with patient prognosis was compared. The method comprises the following specific steps:
(1) Total RNA in the tissue sample is extracted.
(2) Expression of RETSAT was detected using qRT-PCR: provided by assist Saint Co LtdQPCR SYBR GREEN MASTER Mix was detected on a QuantStudio fluorescent quantitative PCR apparatus supplied by Thermo Fisher, the primer sequences were: RETSAT: forward: TACTTGGGACTATTCTCTGGCA, reverse: TACTTGGGACTATTCTCTGGCA; reference gene GAPDH: forward: AGAAGGCTGGGGCTCATTTG, reverse: AGGGGCCATCCACAGTCTTC. The primers are all provided by Shanghai Biotechnology Co.
(3) Patient survival was followed (> 5 years). The follow-up period is once a year, with a maximum follow-up time of 10 years.
(4) And (5) analyzing the detection result by a survival curve. The median 8.089 of the delta CT values of RETSAT relative to the internal reference GAPDH was taken as a cutoff value, so as to distinguish high/low expression groups, and corresponding to different survival conditions, and the result is shown in FIG. 3, and for a patient with lung adenocarcinoma treated by cisplatin, the tumor tissue sample has high expression of RETSAT, which means better prognosis, indicating that the patient has good response to cisplatin. Thus, RETSAT expression levels can be used to predict the susceptibility of a lung adenocarcinoma patient to cisplatin treatment. Meanwhile, the Harrell's c-index calculated by RETSAT expression level applied to the cox proportional hazards regression model is 0.681, which indicates that the prediction sensitivity and specificity are good.
Thus, the results of the present invention demonstrate that: detecting RETSAT expression in a tumor sample of a patient with lung adenocarcinoma, wherein if RETSAT expression in the sample is low (i.e., delta CT > 8.089), the patient is resistant to cisplatin chemotherapy; if RETSAT is expressed high (i.e., ΔCT is less than or equal to 8.089), then the patient is resistant to cisplatin.
The above-described embodiments are only preferred embodiments of the present invention, and are not intended to be limiting in any way and in nature, and it should be noted that several modifications and additions may be made to those skilled in the art without departing from the invention, which modifications and additions are also intended to be construed as within the scope of the invention.
Claims (1)
1. The application of a reagent for detecting RETSAT expression quantity in preparing and detecting a kit for evaluating the sensitivity of cisplatin to lung adenocarcinoma is provided.
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| CA2630597A1 (en) * | 2005-12-08 | 2007-06-14 | Novartis Ag | Effects of inhibitors of fgfr3 on gene transcription |
| WO2013142571A2 (en) * | 2012-03-20 | 2013-09-26 | Cornell University | Assays for the identification of compounds that modulate lipid homeostasis |
| CN106822898B (en) * | 2017-02-17 | 2018-09-25 | 王晓华 | Application of the STAT3 gene expressions in terms of improving adenocarcinoma of lung chemosensitivity is lowered in targeting |
| US20230053540A1 (en) * | 2019-02-19 | 2023-02-23 | Massachusetts Institute Of Technology | Treatment of liver injury |
| CN110499364A (en) * | 2019-07-30 | 2019-11-26 | 北京凯昂医学诊断技术有限公司 | A kind of probe groups and its kit and application for detecting the full exon of extended pattern hereditary disease |
| CN113295815A (en) * | 2021-05-24 | 2021-08-24 | 南京鼓楼医院 | Marker molecules of different time points of endometrial secretory phase and screening method thereof |
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| Title |
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| Retinol Saturase Mediates Retinoid Metabolism to Impair a Ferroptosis Defense System in Cancer Cells;Guoshu Bi 等;Cancer Research;20230715;第83卷;2387-2404 * |
| RETSAT associates with DDX39B to promote fork restarting and resistance to gemcitabine based chemotherapy in pancreatic ductal adenocarcinoma;Qiu Tu等;J Exp Clin Cancer Res;20220915;第41卷;274 * |
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