Interaction of Thiophene and Their Derivatives with BRCA-1 Using a Theoretical Model

Lauro Figueroa-Valverde; Rosas-Nexticapa Marcela; Magdalena Alvarez-Ramirez; Maria Lopez-Ramos; Virginia Mateu-Armand; Hernandez-Vazquez Patricia

doi:10.51847/4AnibsrLIW

ARTICLE

Year: 2024 | Volume: 13 | Issue: 2 | Page: 40-44 View issue

Interaction of Thiophene and Their Derivatives with BRCA-1 Using a Theoretical Model

Lauro Figueroa-Valverde , Rosas-Nexticapa Marcela , Magdalena Alvarez-Ramirez , Maria Lopez-Ramos , Virginia Mateu-Armand^*✉ , Hernandez-Vazquez Patricia

Abstract

Several studies indicate that breast cancer has been associated with increases in mortality rates worldwide. There are several risk factors to developed breast cancer such as obesity, high fat diet, Lack of physical activity, alcohol, use of oral contraceptives, genetic mutations, and others. In addition, some reports suggesting that breast cancer gene 1 (BRCA1) has been related to breast cancer development. This research aimed to determine the possible interaction of thiophene (1) and their analogs (2 to 25) with BRCA-1 using the 3pxb protein and niraparib drug as controls in a docking model The results showed differences in the interaction of thiophene and its analogs with the surface of the 3pxb protein compared to niraparib drug. Besides, other data indicate that the inhibition constant (Ki) associated with thiophene-derivatives-protein complex formation for 11, 13, 16, 18, and 20 was similar manner to Ki for niraparib. These data suggest that compounds 11, 13, 16, 18, and 20 could inhibit the biological activity of BRCA-1; this phenomenon can be translated as a decrease in breast cancer cell growth.

Keywords: Cancer, Thiophene, Derivatives, BRCA-1

Introduction

For several years, breast cancer has increased drastically in women, which has increased the mortality rate worldwide.^{[1, 2]} Some risk factors involved in the development of breast cancer have been detected, such as demographic, reproductive, hormonal, hereditary, and lifestyle parameters.^[3] It should be noted that different drugs have been used to treat breast cancer such as tamoxifen (estrogen-receptor inhibitor),^[4] trastuzu-mab,^[5] pertuzumab,^[6] margetuximab,^[7] lapatinib,^[8] neratinib/fulvestrant,^[9] tucati-nib,^[10] everolimus,^[11] alpelisib,^[12] capiva-sertib/fulvestrant,^[13] and olaparib.^[14] Nevertheless, some drugs produce some adverse effects such as nausea, diarrhea, and neutropenia.^[15] In the search for new pharmacological alternatives, several drugs have been developed to treat breast cancer; for example, the preparation of niraparib (MK-4827) as an ADP-ribose polymerase inhibitory agent which is effective in BRCA-1 and BRCA-2 mutant tumors.^[16] In addition, types of drugs such as olaparib and talazoparib were approved to treat breast cancers that express either BRCA-1 or BRCA-2 mutations.^[17] Furthermore, a study in a phase III clinical trial showed that both olaparib and talazoparib drugs can produce beneficial effects in patients with breast cancer.^[18] Other data showed that a benzo[a]pyrene and its epoxide diol can produce changes in BRCA-1 expression.^[19] Furthermore, a study indicates that a carboxamide derivative has activity in a breast cancer cell line (MDA-MB-436; BRCA-1 mutated).^[20]

On the other hand, some thiophene derivatives were synthesized to evaluate their biological activity against breast cancer; in this way, a study showed the preparation of a chloro-benzothiophene analog with biological activity against a breast cancer cell line (MCF-7).^[21] Other report indicate that a thiophene derivative (4-Methyl-5-(phenyldiazenyl)-2-[((1-(thio- phen-2-yl) ethylidene)hydrazineylidene]- thiazol-3(2H)amine) decrease growth cancer using MCF-7 cells.^[22] Other data displayed that a thiophene analog (pyrimido-thieno-pyrimidine derivative) decreases cancer cell line growth MCF-7 and A549 through epidermal growth factor receptor inhibition.^[23] Besides, a dioxo-benzo[b]-thiophene derivative was developed as an agent YAP-TEAD (transcript-tional regulators) inhibitor for treating breast cancer using a cancer cell model.^[24] Another report showed that a

thiophene-triazine derivative decreased the growth of MCF-7 cancer cells through PI3K/mTOR (phosphoinositide 3-kinase/mammalian target of rapamycin) pathway inhibition.^[25] All these experimental data indicate that some thiophene derivatives can inhibit breast cancer growth; nevertheless, its coupling with some biomolecules involved in cell growth in breast cancer patients is unclear. Therefore, this study aimed to determine the possible interaction of several thiophene (compound 1) and their analogs (2 to 25) with BRCA-1 (breast cancer gene 1) using a theoretical model.

Materials and Methods

Figure 1 shows the chemical structure of thiophene and its analogs which were used to determine its possible interaction with the BRCA-1 gene surface as follows:

Figure 1. Chemical structure of thiophene (1) and its derivatives (2-25).

1 = Thiophene

2 = 1-Benzothiophene-4-ol

3 = 1-Methylbenzo(b)naphtho(1,2-d)-thiophene

4= 2-([(E)-(3,5-Dichloro-2-hydroxyphenyl)methylidene]amino)-5,6-dihydro-4H-cyclopenta[b]thiophene-3-carbonitrile

5 = 2-(1H-Imidazol-1-ylmethyl)-4,5-dihydrobenzo(b)thiophene-6-carboxylic acid

6 = 2-(Chloromethyl)-thiophene

7 = 2-(tert-butoxy)thiophene

8 = 2,2,3-Trifluoro-2,4,5,6,7,8-hexahydrocyclohepta(b)thiophene

9 = 2,5-Dimethyltetrahydrothiophene

10 = 3-(2-(Dimethylamino)ethyl)-5-methoxybenzo(b)thiophene

11 = 3-(2-(Dimethylamino)ethyl)benzo(b)thiophene

12 = 3-(2-(Methylamino)ethyl)benzo(b)thiophene

13 = 3-(2-Aminoethyl)-5-methoxybenzo(b)thiophene

14 = 3-Formylthiophene

15 = 3-Methylbenzo(b)naphtho(1,2-d)thiophene

16 = 3-Nitrobenzo(b)thiophene

17 = 4-Methylbenzo(b)naphtho(2,3-d)thiophene

18 = 5-Bromo-2-(4-fluoro-phenyl)-3-(4-methanesulfonyl-phenyl)-thiophene

19 = 6-Methylbenzo(b)naphtho(2,1-d)thiophene

20 = 6-Methylbenzo(b)thiophene

21 = -Benzothiophene 1,1-dioxide

22 = Tetrahydro-thiophene-1-oxide

23= N-[[4-[(thiophene-2-carbonylamino)carbamoyl]cyclohexyl]methyl]thiophene-2-sulfonamide

24 = Naphtho(2,1-b)thiophene

25= 19-thiapentacyclo[14.2.1.05,18.06,11.012,17]nonadeca-1,3,5(18), 6,8,10, 12(17),13,15-nonaene

Ligand-protein complex

Coupling of thiophene and its derivatives with BRCA-1 was evaluated using 3pxb^[26] protein and niraparib (MK-4827) as theoretical tools in DockingServer software.^[27]

Pharmacokinetics parameter

Some pharmacokinetic parameters for thiophene derivatives (11, 13, 16, 18, and 20) were evaluated using the SwissADME software.^[28]

Toxicity analysis

Possible toxicity induced through different administration routes of thiophene derivatives (11, 13, 16, 18, and 20) and niraparib was evaluated using the GUSAR program.^[29]

Results and Discussion

Some reports indicate that several thiophene derivatives can exert biological activity against cancer cells;^[21-25] nevertheless, experimental results are very confusing. Analyzing these data, this study aimed to evaluate the possible interaction of some thiophene and its derivatives with some biomolecules involved in cancer cell growth such as BRCA-1 using 3pxb protein and niraparib as theoretical tools in a Docking model. The results (Table 1 and Figure 2) showed that LJH685 interacts with different amino acid residues (Leu₁₆₇₉; Ile₁₆₈₀; Arg₁₆₉₉; Ala₁₇₀₀; Leu₁₇₀₁; Lys₁₇₀₂; Leu₁₇₀₅; Gln₁₇₇₉) involved in the 3pxb protein surface in comparison with thiophene (1) and its derivatives (2 to 25). This data indicates that the coupling of thiophene and its analogs with the 3pxb protein surface can depend on the chemical characteristic of each compound (Table 1 and Figure 2) or different thermodynamics parameters involved in the thiophene-protein complex formation.

Table 1. Theoretical interaction of thiophene (1) and its analogs (compounds 2-25) with 3pxb protein surface
Compound	Aminoacid residues
Niraparib	Leu₁₆₇₉; Ile₁₆₈₀; Arg₁₆₉₉; Ala₁₇₀₀; Leu₁₇₀₁; Lys₁₇₀₂; Leu₁₇₀₅; Gln₁₇₇₉
1	Ile₁₆₈₀; Leu₁₇₀₁; Lys₁₇₀₂; Leu₁₇₀₅; Gln₁₇₇₉
2	Glu₁₆₉₈; Arg₁₆₉₉; Val₁₇₄₀; Val₁₇₄₁
3	Glu₁₆₉₈; Arg₁₆₉₉; Ala₁₇₀₀; Asn₁₇₇₄; Met₁₇₇₅; Arg₁₆₉₉;Leu₁₈₃₉
4	Arg₁₆₉₉; Ala₁₇₀₀; Leu₁₇₀₁; Lys₁₇₀₂; Asn₁₇₇₄; Met₁₇₇₅
5	Ser₁₆₅₅; Ala₁₇₀₀; Leu₁₇₀₁; Lys₁₇₀₂; Phe₁₇₀₄; Asn₁₇₇₄; Met₁₇₇₅;Arg₁₈₃₅; Leu₁₈₃₉
6	Arg₁₆₉₉; Phe₁₇₀₄; Asn₁₇₇₄; Met₁₇₇₅; Arg₁₈₃₅; Leu₁₈₃₉
7	Leu₁₇₀₁; Phe₁₇₀₄; Asn₁₇₇₄; Met₁₇₇₅;Arg₁₈₃₅; Leu₁₈₃₉
8	Arg₁₆₉₉; Leu₁₇₀₁; Phe₁₇₀₄; Met₁₇₇₅; Leu₁₈₃₉
9	Phe₁₇₀₄; Asn₁₇₇₄; Met₁₇₇₅; Arg₁₈₃₅; Leu₁₈₃₉
10	Glu₁₆₉₈; Arg₁₆₉₉; Phe₁₇₀₄; Met₁₇₇₅
11	Glu₁₆₉₈; Ala₁₇₀₀; Leu₁₇₀₁
12	Glu₁₆₉₈; Arg₁₆₉₉; Phe₁₇₀₄; Met₁₇₇₅; Leu₁₈₃₉
13	Glu₁₆₉₈; Ala₁₇₀₀; Leu₁₇₀₁
14	Ile₁₆₈₀; Leu₁₇₀₁; Lys₁₇₀₂; Leu₁₇₀₅
15	Glu₁₆₉₈; Arg₁₆₉₉; Ala₁₇₀₀; Met₁₇₇₅; Leu₁₈₃₉
16	Arg₁₆₉₉; Leu₁₇₀₁; Phe₁₇₀₄; Met₁₇₇₅; Leu₁₈₃₉
17	Ala₁₇₀₀; Leu₁₇₀₁; Met₁₇₇₅; Arg₁₈₃₅; Leu₁₈₃₉
18	Glu₁₆₉₈; Arg₁₆₉₉; Ala₁₇₀₀; Val₁₇₄₀; Val₁₇₄₁; Thr₁₇₇₃; Asn₁₇₇₄; Met₁₇₇₅; Arg₁₈₃₅
19	Arg₁₆₉₉; Ala₁₇₀₀; Leu₁₇₀₁; Met₁₇₇₅; Leu₁₈₃₉
20	Arg₁₆₉₉; Leu₁₇₀₁; Phe₁₇₀₄; Asn₁₇₇₄; Met₁₇₇₅; Arg₁₈₃₅; Leu₁₈₃₉
21	Arg₁₆₉₉; Phe₁₇₀₄; Asn₁₇₇₄; Met₁₇₇₅; Leu₁₈₃₉
22	Ile₁₆₈₀; Leu₁₇₀₁; Lys₁₇₀₂; Leu₁₇₀₅
23	Ser₁₆₅₅; Glu₁₆₉₈; Arg₁₆₉₉; Ala₁₇₀₀; Leu₁₇₀₁; Asn₁₇₇₄; Met₁₇₇₅
24	Arg₁₆₉₉; Leu₁₇₀₁; Phe₁₇₀₄; Met₁₇₇₅; Leu₁₈₃₉
25	Glu₁₆₉₈; Arg₁₆₉₉; Leu₁₇₀₁; Met₁₇₇₅; Leu₁₈₃₉

Figure 2. Binding of thiophene analogs (11, 13, 16, 18, and 20) with the 3xpb protein surface. Visualized with GL mol viewer, DockingServer.

Thermodynamic parameters

There are theoretical studies that suggest that coupling of some drugs with several biomolecules may depend on different thermodynamic parameters, such as binding free energy, electrostatic energy, total intermolecular energy, Van Der Waals (vdW) + hydrogen bond (H bond) + desolvation energy.^[29] For this reason, the study of these thermodynamic parameters involved in the interaction of thiophene and its analogs with the 3pxb protein surface was determined. The results (Table 2) displayed different energy levels for thiophene, and its analogs in comparison with niraparib. Furthermore, the inhibition constant (Ki) was higher for thiophene and its analogs 2-10, 12, 14, 15, 17, 19, and 21-25 compared to niraparib. However, Ki for thiophene analogs 11, 13, 16, 18, and 20 was very similar to the niraparib drug. These data suggest that thiophene derivatives 11, 13, 16, 18, and 20 could act as BRCA-1 inhibitory agents. However, it is important to mention that other types of biological experiments are required to verify this hypothesis.

Table 2. Thermodynamic parameters for thiophene-3pxb-protein complex formation
Compound	A	B	C	D	E	F
Niraparib	-3.97	1.23	-4.45	0.17	-4.28	566.74
1	-2.69	10.64	-2.69	-0.01	-2.69	262.81
2	-3.20	4.52	-3.30	-0.19	-3.50	361.44
3	-5.71	65.54	-5.70	-0.01	-5.71	507.69
4	-5.15	166.84	-6.00	0.05	-5.95	639.36
5	-4.89	259.58	-5.42	-0.36	-5.78	502.05
6	-3.12	5.17	-3.41	-0.01	-3.42	324.30
7	-3.02	6.15	-3.70	0.01	-3.69	394.77
8	-5.29	132.58	-5.20	-0.09	-5.29	366.08
9	-3.09	5.39	-3.10	0.01	-3.09	312.43
10	-4.46	540.66	-4.50	-0.97	-5.47	479.82
11	-4.00	1.17	-3.98	-0.77	-4.76	410.80
12	-4.44	560.34	-4.11	-1.15	-5.26	426.31
13	-3.92	1.33	-3.92	-1.17	-5.09	434.79
14	-2.87	7.87	-3.12	-0.05	-3.17	293.08
15	-5.00	216.89	-4.99	0.00	-5.00	507.79
16	-3.77	1.74	-4.01	-0.05	-4.06	368.70
17	-5.09	186.30	-5.09	0.00	-5.09	493.21
18	-4.07	1.04	-5.12	-0.03	-5.14	559.29
19	-5.01	211.98	-5.01	0.00	-5.01	485.12
20	-3.72	1.89	-3.69	-0.02	-3.72	383.12
21	-3.40	3.22	3.38	-0.02	-3.40	372.32
22	-2.67	11.10	-2.65	0.02	-2.67	276.73
23	-2.30	20.55	-4.32	0.10	-4.21	616.39
24	-4.16	888.00	-4.15	-0.01	-4.15	402.99
25	-5.48	96.79	-5.47	0.00	-5.48	497.96

A = Est: Free Energy of Binding (kcal/mol)

B = Est. Inhibition Constant, Ki (mM)

C = vdW + Hbond + desolv Energy (kcal/mol)

D = Electrostatic Energy (kcal/mol)

E = Total Intermolec. Energy (kcal/mol)

F = Interact. Surface

Pharmacokinetic evaluation

Several methods have been used to determine some pharmacokinetic parameters to evaluate the possible biological activity of different drugs.^[30-33] For this reason, this research aimed to determine some pharmacokinetic parameters that could be involved in the administration of thiophene analogs 11, 13, 16, 18, 20, and nirapib using the SwissADME program (Table 3). The results showed differences in gastrointestinal absorption degree and metabolism (which involves various types of cytochromes P450 enzymes) for thiophene 11, 13, 16, 18, and 20 compared to the niraparib drug. Possibly this process could be associated with the different chemical characteristics of each thiophene analog and differences in its lipophilicity degree.

Table 3. Theoretical analysis of some pharmacokinetic factors for thiophene analogs and niraparib drug

Parameter

Niraparib

GI absorption

BBB permeant

P-GP substrate

CYP1A2 inhibitor

CYP2C19 inhibitor

CYP2C9 inhibitor

CYP2D6 inhibitor

CYP3A4 inhibitor

Consensus LogP_O/_W

High

Yes

2.29

High

Yes

3.14

High

Yes

2.49

High

Yes

2.02

Low

Yes

5.17

High

Yes

3.19

Toxicity analysis

Some reports suggest that different thiophene derivatives may produce some toxicity degree using several biological models.^[34-37] This research aimed to evaluate the possible toxicity produced by thiophene analogs (11, 13, 16, 18, and 20) using the GUSAR software.^[28] The results suggest (Table 4) that thiophene derivative 18 possibly requires high doses to produce toxicity (LD50) via intraperitoneal, intravenous, oral, and subcutaneous compared to the niraparib drug. Besides, compound 16 requires a higher dose through the oral route compared to niraparib. All these data indicate that the toxicity degree would depend on the dose and administration route of each thiophene analog.

Table 4. Theoretical analysis of toxicity for thiophene derivatives (11, 13, 16, 18, and 20) and niraparib drug using GUSAR Software
Compound	IP LD50 (mg/kg)	IV LD50 (mg/kg)	Oral LD50 (mg/kg)	SC LD50 (mg/kg)
Niraparib	423.10	104.50	366.00	158.60
11	90.10	31.09	190.60	150.50
13	189.80	75.37	1154.00	374.60
16	216.20	115.80	868.40	181.00
18	586.60	285.20	465.80	307.50
20	227.60	63.58	1232.00	416.20

IP - Intraperitoneal route of administration

IV - Intravenous route of administration

Oral - Oral route of administration

SC - Subcutaneous route of administration

Conclusion

In this study, the possible coupling of thiophene and its analogs with the 3pxb protein surface. The results indicate that thiophene derivatives 11, 13, 16, 18, and 20 may interact with some amino acid residues involved in the 3pxb protein surface. This data suggests that thiophene derivatives 11, 13, 16, 18, and 20 could act as BRCA-1 gene inhibitor agents; this phenomenon could be translated as a decrease in breast cancer cell growth. Analyzing these data these thiophene derivatives may be considered good pharmacological agents to treat breast cancer.

Acknowledgments

None.

Conflict of interest

None.

Financial support

None.

Ethics statement

All procedures in this study were performed in accordance with protocols for Pharmacochemistry Laboratory of University Autonomous of Campeche.

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Vancouver

Figueroa-Valverde L, Marcela R, Alvarez-Ramirez M, Lopez-Ramos M, Mateu-Armand V, Patricia H. Interaction of Thiophene and Their Derivatives with BRCA-1 Using a Theoretical Model. Clin Cancer Investig J. 2024;13(2):40-4. https://doi.org/10.51847/4AnibsrLIW

APA

Figueroa-Valverde, L., Marcela, R., Alvarez-Ramirez, M., Lopez-Ramos, M., Mateu-Armand, V., & Patricia, H. (2024). Interaction of Thiophene and Their Derivatives with BRCA-1 Using a Theoretical Model. Clinical Cancer Investigation Journal, 13(2), 40-44. https://doi.org/10.51847/4AnibsrLIW

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