An organic molecule for light-controlled release of nitric oxide and its preparation and application in inhibiting tumor EMT

Abstract

The present invention belongs to the field of chemistry and biomedical technology, and in particular to a preparation of an organic molecule for light-controlled release of nitric oxide and its application in inhibiting tumor epithelial-mesenchymal transition (EMT). The present invention has developed and designed an organic molecule for light-controlled release of nitric oxide, which contains a benzimidazole group and a light-triggered nitric oxide releasing group. The molecule has aggregation-induced luminescence characteristics, which can realize wash-free cell imaging, and can exert the tumor-suppressing effect of benzimidazole in the absence of light. After releasing nitric oxide under light triggering, the tumor EMT process can be further regulated, and the two can synergistically induce cancer cell death. The organic molecule for light-controlled release of nitric oxide provided by the present invention is developed and applied to biological research for the first time, and provides a new idea for developing new nitric oxide donors and cancer treatment strategies.

Description

Technical Field

[0001] The present invention belongs to the technical field of chemistry and biomedicine, and specifically relates to an organic molecule for light-controlled release of nitric oxide, as well as its preparation and application in inhibiting tumor EMT. Background Art

[0002] The epithelial-mesenchymal transition (EMT) process is involved in the development and progression of tumors. It is a complex network regulatory mechanism mediated by multiple signaling pathways and transcription factors. It can endow tumor cells with metastatic properties, enhance their invasiveness, and enable them to invade surrounding tissues and colonize distant organs. Therefore, the discovery of new EMT intervention methods is of great significance for cancer treatment.

[0003] Nitric oxide (NO) is a bioactive molecule ubiquitous in the body, playing a key regulatory role in physiological and pathological processes. Studies have shown that NO's regulatory effects are significantly concentration-dependent: at low concentrations, NO can promote important physiological processes such as vasodilation and angiogenesis; at higher concentrations, NO exhibits potential as an anticancer and antimicrobial agent, effectively combating foreign pathogens by stimulating immune responses. Therefore, NO, as a multifunctional therapeutic agent, has garnered extensive attention and intensive research. Currently, studies have confirmed that NO regulates the epithelial-mesenchymal transition (EMT) process. However, due to significant limitations in storage, half-life, and in vivo delivery of NO gas itself, the application of therapeutics solely relying on NO gas is greatly restricted. To address these issues, researchers have developed a variety of NO donors (such as azodiol olefinium and S-nitrosothiol) for NO storage and delivery. These donors exhibit good stability and high in vivo bioavailability, and can spontaneously release NO in a predictable manner under physiological conditions. However, these donors still face several challenges. For example, under the influence of stimuli in the body (such as low pH and glutathione), the release process of NO donors is poorly controllable, has limited penetration, and lacks tumor specificity. In addition, these donors also have the problem of aggregation-induced quenching (AIE), which further affects their performance. Therefore, how to precisely control the time and space of NO release has become a research focus for achieving anti-tumor growth and inhibition of migration and invasion, and is also a key technical problem that needs to be solved in the current field of NO therapy.

[0004] Benzimidazole has structural features similar to purines and can easily interact with biological molecules in living systems. It is a key pharmacophore with a wide range of biological activities and chemotherapeutic effects. Studies have shown that many benzimidazole derivatives have excellent effects in inhibiting tumor growth and migration. Therefore, benzimidazole is considered to be an important basic structural unit in the development of anti-tumor drugs. Given the core role of EMT in cancer progression and the many limitations of current NO therapy in storage, delivery and release, if the powerful anti-cancer effect of NO can be combined with the biological activity of benzimidazole to develop a new drug molecule that inhibits tumor EMT, it will open up a new direction for tumor treatment and have important application prospects and clinical value. Summary of the Invention

[0005] To address the poor controllability and aggregation-induced quenching (ACQ) issues of existing nitric oxide (NO) donors, a novel NO donor was designed and synthesized. This donor not only overcomes the limitations of traditional NO donors but also incorporates aggregation-induced emission (AIE) properties and a benzimidazole group with antitumor activity. This donor can continuously release NO under light stimulation, thereby achieving multiple synergistic antitumor effects in cancer treatment, providing a new strategy with broad application prospects for tumor treatment.

[0006] In order to achieve the above object, the technical solution adopted by the present invention is:

[0007] The present invention provides an organic molecule for light-controlled release of nitric oxide, wherein the organic molecule has a structure as shown in formula (I):

[0008]

[0009] The photocontrolled nitric oxide release donor molecule in formula (I) includes a benzimidazole receptor group having anti-tumor activity and a photocontrolled nitric oxide release donor group, with a maximum absorption wavelength of approximately 368 nm and a maximum emission wavelength of approximately 481 nm; the photocontrolled nitric oxide release donor molecule has aggregation-induced luminescence characteristics; the photocontrolled nitric oxide release donor molecule continuously releases NO under 405 nm laser irradiation.

[0010] The present invention also provides a method for preparing the organic molecule capable of light-controlled release of nitric oxide, comprising the following steps:

[0011] S1. dissolving p-bromoaniline and di-tert-butyl dicarbonate in methanol, and reacting to obtain compound 1;

[0012] S2, dissolving compound 1 and cesium carbonate in N,N-dimethylformamide under anaerobic conditions, and then slowly adding potassium iodide to obtain compound 2 after reaction;

[0013] S3, dissolving compound 2, 5-formyl-2-thiopheneboronic acid, potassium carbonate, and [1,1'-bis(diphenylphosphino)ferrocene]palladium dichloride in a mixed solvent of toluene / methanol / water under anhydrous and oxygen-free conditions, and reacting to obtain compound 3;

[0014] S4, dissolving compound 3, o-phenylenediamine and sodium metabisulfite in N,N-dimethylformamide under anaerobic conditions, and reacting to obtain compound 4;

[0015] S5, dissolving compound 4 in a mixed solvent of dichloromethane and trifluoroacetic acid under anhydrous and oxygen-free conditions, and reacting at room temperature to obtain compound 5;

[0016] S6. dissolving compound 5 in methanol, and then slowly adding concentrated hydrochloric acid and sodium nitrite aqueous solution to obtain an organic molecule that releases nitric oxide under light-controlled conditions;

[0017] The structures of Compound 1, Compound 2, Compound 3, Compound 4, and Compound 5 are shown below:

[0018]

[0019] Preferably, in S1, the molar ratio of p-bromoaniline to di-tert-butyl dicarbonate is 1:1.0-1.5; the reaction temperature is 90-120° C., and the reaction time is 20-24 h.

[0020] Preferably, in S2, the molar ratio of compound 1, cesium carbonate and potassium iodide is 1:1.5-1.8:1.0-1.4; the reaction temperature is room temperature, and the reaction time is 20-24 hours.

[0021] Preferably, in S3, the molar ratio of compound 2, 5-formyl-2-thiopheneboronic acid, and potassium carbonate is 1:1.5-2.5:4-6, the molar ratio of [1,1'-bis(diphenylphosphino)ferrocene]palladium dichloride to compound 2 is 1:0.04-0.06; the volume ratio of toluene, methanol, and water in the mixed solvent is 5-7:1-3:1; the reaction temperature is 80-100°C, and the time is 40-50h.

[0022] Preferably, in S4, the molar ratio of compound 3, o-phenylenediamine and sodium metabisulfite is 1:1:1; the reaction temperature is 110-130° C., and the reaction time is 6-8 h.

[0023] Preferably, in S5, the volume ratio of dichloromethane to trifluoroacetic acid in the mixed solvent is 3-5:1, and the reaction time is 4-5 hours.

[0024] Preferably, in S6, the molar ratio of compound 5 to sodium nitrite is 1:1, and the molar ratio of compound 5 to concentrated sulfuric acid is 1:4-6; the reaction process is: after dissolving compound 5 in methanol, stirring in an ice bath for 10-20 minutes, adding concentrated hydrochloric acid, continuing the reaction for 0.4-0.8 hours, adding sodium nitrite aqueous solution, and reacting in an ice bath in the dark for 1-2 hours.

[0025] The present invention also provides the use of the organic molecule capable of light-controlled release of nitric oxide in the preparation of a cell-free washing imaging agent.

[0026] The donor small molecule (I) provided by the present invention can be quickly taken up by cells and has good biological imaging ability and wash-free function.

[0027] The present invention also provides the use of the organic molecule capable of light-controlled release of nitric oxide in the preparation of anti-tumor drugs.

[0028] The NO donor small molecule (I) provided by the present invention has aggregation-induced luminescence properties, and light-controlled nitric oxide release is achieved. By co-culturing with cancer cells, it can not only inhibit cell activity in the dark, but also further inhibit cell activity by releasing nitric oxide gas under light stimulation, thereby achieving multi-effect anti-tumor effects, thereby achieving the purpose of inducing tumor cell death.

[0029] Preferably, the NO donor molecule (I) inhibits tumor cell growth and / or inhibits tumor EMT process.

[0030] The donor small molecule (I) provided by the present invention not only has an inhibitory effect on the activity of tumor cells, but also can inhibit the EMT process induced by TGF-β in the presence or absence of light, thereby achieving the purpose of anti-tumor metastasis.

[0031] Preferably, the tumor includes (but is not limited to) lung cancer.

[0032] Compared with the prior art, the present invention has the following beneficial effects:

[0033] The present invention combines the characteristics of aggregation-induced emission (AIE) to design and develop a new multi-effect NO donor small molecule that uses light as a trigger source to release nitric oxide (NO). The molecule contains a benzimidazole group with anti-tumor activity and a functional group that triggers the release of NO, and exhibits aggregation-induced emission characteristics. Under no-light conditions, the benzimidazole group exerts its effect of inhibiting tumor growth; under light conditions, the molecule can release NO, and by further regulating the tumor epithelial-mesenchymal transition (EMT) process, it synergizes with benzimidazole to induce cancer cell death and inhibit its metastasis. The present invention successfully constructed a new molecular system containing a benzimidazole group and a light-controlled NO-releasing group, achieving a multi-effect synergistic, controllable release of NO anti-tumor effect. In addition, the light-controlled NO-releasing organic molecule provided by the present invention exhibits good anti-tumor growth and metastasis capabilities, providing a new strategy for the development of new NO donors and cancer treatment. BRIEF DESCRIPTION OF THE DRAWINGS

[0034] Figure 1 This is the H NMR spectrum of the donor molecule (Ⅰ) for light-controlled release of nitric oxide;

[0035] Figure 2 The UV absorption and fluorescence emission diagrams of the donor molecule (Ⅰ) for light-controlled release of nitric oxide;

[0036] Figure 3 NO release diagram of the donor molecule (Ⅰ) for light-controlled release of nitric oxide;

[0037] Figure 4 This is the aggregation-induced emission characteristic diagram of the donor molecule (Ⅰ) for light-controlled release of nitric oxide;

[0038] Figure 5 The anti-A549 tumor cell activity of the donor molecule (Ⅰ) for light-controlled release of nitric oxide;

[0039] Figure 6 Cell imaging of the donor molecule (I) for light-controlled release of nitric oxide;

[0040] Figure 7 Effect of donor molecules for light-controlled release of nitric oxide (I) on the mRNA expression of tumor EMT-related proteins. DETAILED DESCRIPTION

[0041] The following is a further description of specific embodiments of the present invention. It should be noted that the description of these embodiments is intended to facilitate understanding of the present invention and does not constitute a limitation of the present invention. In addition, the technical features involved in the various embodiments of the present invention described below may be combined with each other as long as they do not conflict with each other.

[0042] The experimental methods in the following examples are conventional methods unless otherwise specified, and the experimental materials (such as reagents or instruments) used in the following examples are available through conventional commercial channels unless otherwise specified.

[0043] Example 1: Synthesis of donor molecules for light-controlled release of nitric oxide (I)

[0044] The synthetic route of the donor molecule is as follows:

[0045]

[0046] The specific synthesis method comprises the following steps:

[0047] (1) Synthesis of Compound 1: 1 g (5.8 mmol) of p-bromoaniline and 1.522 g (7 mmol) of di-tert-butyl dicarbonate were dissolved in 15 mL of methanol and heated to 100°C for 20 h. After the reaction, the mixture was cooled to room temperature and separated by column chromatography using a 1:1 (v / v) eluent of PE:DCM to obtain 0.96 g of Compound 1 with a yield of 96%.

[0048] (2) Synthesis of Compound 2: 10 g (0.037 mol) of compound 1 from step (1) and 19.156 g (0.059 mol) of cesium carbonate were added to two reaction bottles in sequence. The mixture was evacuated and 20 mL of N,N-dimethylformamide was added under nitrogen atmosphere. The mixture was stirred at room temperature for 30 min until the solid was completely dissolved. 2.53 mL (0.0407 mol) of potassium iodide was slowly added dropwise and the reaction was continued for 18 h. After the reaction was completed, the mixture was cooled to room temperature and extracted with ethyl acetate and saturated brine (v:v 1:1). The upper organic matter was collected and distilled under reduced pressure to obtain a crude product. The obtained product was separated by chromatography using a chromatographic column with an eluent of PE:DCM = 1:1 (v / v) to obtain 9.4 mL of compound 2 with a yield of 90%.

[0049] (3) Synthesis of compound 3: 1 g (3.49 mmol) of compound 2 from step (2), 1.09 g (6.98 mmol) of 5-formyl-2-thiopheneboronic acid, 2.42 g (17.5 mmol) of potassium carbonate and 0.13 g (0.175 mmol) of catalyst [1,1'-bis(diphenylphosphino)ferrocene]palladium dichloride (CAS No.: 72287-26-4) were added to a reaction flask, and 45 mL of a mixed solvent of toluene / methanol / water (6:2:1, v / v / v) was added under an anhydrous and oxygen-free environment. The temperature was raised to 90°C for reaction for 2 days, and the reaction progress was monitored by TCL. After completion of the reaction, the mixture was extracted with dichloromethane and water (v:v 1:1). The lower organic layer was collected and separated using a chromatography column with an eluent of PE:EA = 5:1 (v / v). The filtrate was collected, concentrated under reduced pressure, and slightly dissolved in methanol. Natural crystallization was performed to obtain 478 mg of compound 3 with a yield of 48%.

[0050] (4) Synthesis of Compound 4: 50 mg (0.158 mmol) of compound 3 from step (3), 17.05 mg (0.158 mmol) of o-phenylenediamine, and 29.98 mg (0.158 mmol) of sodium metabisulfite were added to a reaction flask in sequence. The flask was evacuated and 4 mL of N,N-dimethylformamide was added under a nitrogen atmosphere. The temperature was raised to 130°C and the reaction was allowed to proceed for 6 h. After the reaction, the mixture was extracted with ethyl acetate and saturated brine (v:v 1:1). The filtrate was collected and concentrated under reduced pressure. The reprecipitate was filtered and suctioned to obtain 51 mg of compound 4 with a yield of 80%.

[0051] (5) Synthesis of Compound 5: Under anhydrous and oxygen-free conditions, 5 mL of a mixed solvent of anhydrous dichloromethane / trifluoroacetic acid (4:1, v / v) was added dropwise to 200 mg of Compound 4 from step (4). The reaction was allowed to react at room temperature for 4 h, and the reaction progress was monitored by TLC. After the reaction was completed, the mixture was neutralized with aqueous sodium hydroxide solution and extracted with dichloromethane. The filtrate was concentrated under reduced pressure, and the reprecipitate was filtered to obtain 145 mg of Compound 5, with a yield of 73%.

[0052] (6) Synthesis of Nitric Oxide Donor Small Molecule (I): 43 mg (0.14 mmol) of compound 5 from step (5) was completely dissolved in 2 mL of methanol. After stirring on ice for 10 min, 22 μL (0.7 mmol) of concentrated hydrochloric acid was slowly added dropwise. The reaction was continued for 0.5 h. Then, 10 mg (0.14 mmol) of sodium nitrite aqueous solution was slowly added dropwise. The mixture was allowed to react on ice in the dark for 1 h. After the reaction was completed, the mixture was neutralized with sodium bicarbonate aqueous solution and extracted with dichloromethane. The organic phase was collected to obtain 39 mg of the product with a yield of 91%.

[0053] Reference Figure 1The hydrogen nuclear magnetic spectrum data of the synthesized nitric oxide donor small molecule (Ⅰ) are as follows: 1H NMR (400 MHz, DMSO-D6): δ13.04 (s, 1H), 7.90 (d, J = 8.7 Hz, 2H), 7.85 (d, J = 3.9 Hz, 1H), 7.74 (d, J = 8.6 Hz, 2H), 7.70 (d, J = 3.9 Hz, 1H), 7.63 (d, J = 7.0 Hz, 1H), 7.52 (d, J = 7.3 Hz, 1H), 7.27–7.15 (m, 2H), 3.46 (s, 3H).

[0054] Example 2: Characterization of the donor molecule (I) for light-controlled release of nitric oxide

[0055] (1) Light-controlled nitric oxide release test

[0056] In order to investigate the ability of the photo-controlled nitric oxide release donor molecule (I) to release nitric oxide in vitro, the donor small molecule was prepared into a 30 μM solution and intermittently irradiated with a 405 nm laser to release nitric oxide. The release of nitric oxide was observed by measuring the ultraviolet absorption and fluorescence emission at each time point. Figure 2 As shown in FIG, in the absence of light, the maximum absorption wavelength of the donor molecule for light-controlled release of nitric oxide is about 368 nm, and the maximum emission wavelength is about 481 nm. Figure 3 As shown, as the illumination time increases, the ultraviolet absorption of the donor molecule for light-controlled nitric oxide release red-shifts and the fluorescence intensity gradually increases, reaching a maximum at 210s, indicating that at this time, the release of nitric oxide by the donor molecule for light-controlled nitric oxide release reaches a maximum under light triggering.

[0057] (2) Aggregation-induced emission test

[0058] In order to detect whether the donor molecule (I) for light-controlled release of nitric oxide has aggregation-induced emission properties, the molecule was dissolved in a mixture of dimethyl sulfoxide and toluene with different volume ratios (100%, 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 1% DMSO) and its fluorescence intensity was measured. Figure 4 As shown, with the increase of toluene content, the fluorescence intensity gradually increases, indicating that the donor molecule for light-controlled release of nitric oxide of the present invention has good aggregation-induced emission properties.

[0059] Example 3: Study on the anti-tumor cell proliferation activity of the donor molecule (I) for light-controlled release of nitric oxide

[0060] (1) Cell culture

[0061] The human lung cancer cell line A549 used in this experiment was purchased from ATCC. DMEM high-glucose medium (containing 10% fetal bovine serum, 1% 100 μg / mL streptomycin, and 100 U / mL penicillin) was purchased from GiBco. Cells were incubated in a sterile incubator at 37°C with 5% CO2 and 95% humidity.

[0062] (2) Detection of the anti-tumor cell proliferation activity of the donor molecule (I) for light-controlled release of nitric oxide

[0063] In this study, the MTT assay was used to analyze the effect of the photosensitive nitric oxide donor molecule (I) on the activity of lung cancer A549 cells. When A549 cells grew to about 80% of normal culture, the cell density was diluted to 5×10 4 Cells were plated at 100 μL per well in a 96-well plate. When cells adhered to 40%-50% of the plate, different concentrations of NO donor solution (10, 20, and 50 μM) were added to the experimental groups, while the control group received culture medium containing the same amount of DMSO. After incubation in an incubator for 3 hours, the medium containing the molecule was discarded and replaced with 1× PBS. The cells were illuminated with 405 nm LED light for 1 minute, and fresh culture medium was added to continue incubation for 24 hours. Protected from light, 50 μL of MTT solution was added to each well, and the cells were incubated for 2-4 hours. After gently aspirating the waste solution, 150 μL of DMSO solution was added to each well. The OD value at 490 nm was measured using a microplate reader to calculate the cell growth inhibition rate of the NO donor.

[0064] The results are as follows Figure 5 As shown, in the absence of light, the NO donor inhibited the activity of A549 cells in a concentration-dependent manner. Furthermore, illumination further enhanced this inhibitory effect. The NO donor's inhibitory effect on cancer cells plays the role of benzimidazole in the absence of light, and further exerts a killing effect by releasing NO after illumination, with the two synergistically inducing cancer cell death. These results demonstrate that the nitric oxide donor of the present invention has a growth inhibitory effect on lung cancer cells and exhibits excellent anti-tumor proliferation ability.

[0065] (3) Cellular imaging of donor molecules (I) for photo-controlled release of nitric oxide

[0066] When A549 cells grew to about 80%, cells were plated at 3×10 4 Cells were plated in a confocal dish, cultured overnight, and 10 μM nitric oxide donor small molecules were added. After 30 min of incubation in the dark, cells were washed with PBS or not, and the cell morphology and fluorescence intensity were observed under a laser scanning confocal microscope. Figure 6As shown, the outline of the cells can be significantly observed with strong fluorescence both when washed with PBS and when not washed, indicating that the donor molecule for light-controlled release of nitric oxide in the present invention has a good cell imaging effect and is wash-free.

[0067] Example 4: Study on the regulation of tumor EMT by light-controlled release of nitric oxide donor molecules (I)

[0068] (1) EMT model construction and donor small molecule intervention

[0069] Normally cultured A549 cells were plated at 2×10 5 Cells were evenly distributed in 6-well plates. After overnight culture, the experimental group was pretreated with 5 ng / mL TGF-β for 2 days to induce EMT. Subsequently, 10 μM nitric oxide donor small molecule (I) was added for 3 hours, and fresh culture medium was replaced for an additional 24 hours. The illumination group was illuminated with 405 nm LED light for 1 minute before replacing the culture medium.

[0070] (2) Effects of light-controlled nitric oxide donor molecules (I) on the expression of EMT-related protein mRNA

[0071] RNA was extracted from the samples using a total RNA extraction kit and transcribed into cDNA using a reverse transcription kit. SYBR dye was then used for qRT-PCR amplification. Using GAPDH expression as a control, the mRNA levels of EMT-related marker proteins E-cadherin, N-cadherin, and Vimentin were calculated. qRT-PCR assays were performed to measure the mRNA levels of EMT-related marker proteins E-cadherin, N-cadherin, and Vimentin, as described in the following paper:

[0072] (1)Jugang Wu, Jiwei Yu, Yan Gu, SETD1A to induce epithelial-mesenchymal transition to promote invasion and metastasis through epigenetic reprogramming of snail in gastric cancer, Journal of Clinical Oncology, 2021, 39, 241-241. (2)Pengda Sun, Dong Sun, Xudong Wang, Effects of Scutellaria barbata polysaccharide on the proliferation, apoptosis and EMT of human colon cancer HT29 Cells, Carbohydrate Polymers, 2017, 167, 90-96. (3)Lucile Astorgues-Xerri, Eric Raymond, Sandrine Faivre, Caroline Halimi, Annemilai Tijeras-Raballand, Maria Eugenia Riveiro, Sebastien Albert, Maria Serova, Anne Couvelard, Muriel Hourseau, Armand de Gramont, Abstract A66: Galectin-1 expression correlated with mesenchymal differentiation and resistance to chemotherapy in carcinoma cells, Clinical Cancer Research, 2012, 18, A66.

[0073] The results are as Figure 7As shown, TGF-β pretreatment reduced E-cadherin expression and increased N-cadherin and Vimentin expression in A549 cells, indicating that TGF-β successfully induced EMT in A549 cells. Intervention with a nitric oxide donor small molecule (I) and subsequent release of nitric oxide by light significantly inhibited the effects of TGF-β, increasing E-cadherin expression and decreasing N-cadherin and Vimentin expression. This indicates that the light-controlled release of nitric oxide donor molecules in the present invention can inhibit the tumor EMT process, thereby achieving the purpose of anti-tumor metastasis.

[0074] The embodiments of the present invention are described in detail above, but the present invention is not limited to the described embodiments. It is apparent to those skilled in the art that various changes, modifications, substitutions, and variations of these embodiments may be made without departing from the principles and spirit of the present invention, and the changes still fall within the scope of protection of the present invention.

Claims

1. An organic molecule for light-controlled release of nitric oxide, characterized in that: It has the structure shown in formula (I): 。 2. The method for preparing an organic molecule capable of light-controlled release of nitric oxide according to claim 1, wherein: The following steps are involved: S1. dissolving p-bromoaniline and di-tert-butyl dicarbonate in methanol, and reacting to obtain compound 1; S2, dissolving compound 1 and cesium carbonate in N,N-dimethylformamide under anaerobic conditions, and then slowly adding potassium iodide to obtain compound 2 after reaction; S3, dissolving compound 2, 5-formyl-2-thiopheneboronic acid, potassium carbonate, and [1,1'-bis(diphenylphosphino)ferrocene]palladium dichloride in a mixed solvent of toluene / methanol / water under anhydrous and oxygen-free conditions, and reacting to obtain compound 3; S4, dissolving compound 3, o-phenylenediamine and sodium metabisulfite in N,N-dimethylformamide under anaerobic conditions, and reacting to obtain compound 4; S5, dissolving compound 4 in a mixed solvent of dichloromethane and trifluoroacetic acid under anhydrous and oxygen-free conditions, and reacting at room temperature to obtain compound 5; S6. dissolving compound 5 in methanol, and then slowly adding concentrated hydrochloric acid and sodium nitrite aqueous solution to obtain an organic molecule that releases nitric oxide under light-controlled conditions; The structures of Compound 1, Compound 2, Compound 3, Compound 4, and Compound 5 are shown below: 。 3. The method for preparing organic molecules for light-controlled release of nitric oxide according to claim 2, characterized in that: In S2, the molar ratio of compound 1, cesium carbonate and potassium iodide is 1:1.5-1.8:1.0-1.4; the reaction temperature is room temperature, and the reaction time is 20-24 h.

4. The method for preparing organic molecules capable of light-controlled release of nitric oxide according to claim 2, wherein: In S3, the molar ratio of compound 2, 5-formyl-2-thiopheneboronic acid, and potassium carbonate is 1:1.5-2.5:4-6, and the molar ratio of [1,1'-bis(diphenylphosphino)ferrocene]palladium dichloride to compound 2 is 1:0.04-0.06; the volume ratio of toluene, methanol, and water in the mixed solvent is 5-7:1-3:1; the reaction temperature is 80-100°C, and the reaction time is 40-50 h.

5. The method for preparing organic molecules capable of light-controlled nitric oxide release according to claim 2, wherein: In S4, the molar ratio of compound 3, o-phenylenediamine and sodium metabisulfite is 1:1:1; the reaction temperature is 110-130°C, and the reaction time is 6-8 h.

6. The method for preparing organic molecules capable of light-controlled nitric oxide release according to claim 2, wherein: In S5, the volume ratio of dichloromethane to trifluoroacetic acid in the mixed solvent is 3-5:1, and the reaction time is 4-5 h.

7. The method for preparing organic molecules capable of light-controlled nitric oxide release according to claim 2, wherein: In S6, the molar ratio of compound 5 to sodium nitrite is 1:1, and the molar ratio of compound 5 to concentrated hydrochloric acid is 1:4-6. The reaction process is as follows: compound 5 is dissolved in methanol, stirred in an ice bath for 10-20 min, concentrated hydrochloric acid is added, and the reaction is continued for 0.4-0.8 h. After adding sodium nitrite aqueous solution, the reaction is carried out in an ice bath in the dark for 1-2 h.

8. Use of the organic molecule capable of light-controlled release of nitric oxide according to claim 1 in the preparation of a cell imaging agent, characterized in that: The cells are A549 cells.

9. Use of the organic molecule capable of light-controlled release of nitric oxide according to claim 1 in the preparation of anti-tumor drugs, characterized in that: The tumor is lung cancer.

10. The use according to claim 9, characterized in that The anti-tumor drug inhibits the growth of tumor cells and / or inhibits the EMT process of tumors.

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