Regulatory and therapeutic implications of competing endogenous RNA network in breast cancer progression and metastasis: A review.

Breast cancer (BC) is a global health concern, and development of diagnostic tools and targeted treatments for BC remains challenging. Therapeutic approaches for BC often involve a combination of surgery, radiation therapy, chemotherapy, targeted therapy, and hormone therapy. In recent years, there has been a growing interest in the role of noncoding RNAs (ncRNAs), including long ncRNAs (lncRNAs) and microRNAs (miRNAs), in BC and their therapeutic implications. Various biological processes such as cell proliferation, migration, and apoptosis rely on the activities of these ncRNAs, and their dysregulation has been implicated in BC progression. The regulatory function of the competitive endogenous RNA (ceRNA) network, which comprises lncRNAs, miRNAs, and mRNAs, has been the subject of extensive pathophysiological research. Most lncRNAs serve as molecular sponges for miRNAs and sequester their activities, thereby regulating the expression of target mRNAs and contributing to the promotion or inhibition of BC progression. This review summarizes recent findings on the role of ceRNA networks in BC progression, metastasis, and therapeutic resistance, and highlights the association of ceRNA networks with transcription factors and signaling pathways. Understanding the ceRNA network can lead to the discovery of biomarkers and targeted treatment methods to prevent the spread and metastasis of BC.

In vivo validation of the functional role of MicroRNA-4638-3p in breast cancer bone metastasis.

PURPOSE: Skeletal metastases are increasingly reported in metastatic triple-negative breast cancer (BC) patients. We previously reported that TGF-ß1 sustains activating transcription factor 3(ATF3) expression and is required for cell proliferation, invasion, and bone metastasis genes. Increasing studies suggest the critical regulatory function of microRNAs (miRNAs) in governing BC pathogenesis. TGF-ß1 downregulated the expression of miR-4638-3p, which targets ATF3 in human BC cells (MDA-MB-231). In the present study, we aimed to identify the functional role of miR-4638-3p in BC bone metastasis by the caudal artery injection of the MDA-MB-231 cells overexpressing mir-4638 in the mice. METHODS: MDA-MB-231 cells overexpressing miR-4638 were prepared by stable transfections. Reverse transcriptase quantitative PCR was carried out to determine the expression of endogenous miR-4638-3p and bone resorption marker genes. X-ray, micro-CT, and Hematoxylin & Eosin studies were used to determine osteolytic lesions, trabecular structure, bone mineral density, and micrometastasis of cells. RESULTS: The mice injected with MDA-MB-231 cells overexpressing miR-4638-3p decreased the expression of bone resorption marker genes, compared to MDA-MB-231 cells injection. Reduced osteolytic lesions and restored bone density by MDA-MB-231 cells overexpressing miR-4638-3p were observed. Similarly, the mice injected with MDA-MB-231 cells overexpressing miR-4638-3p showed a better microarchitecture of the trabecular network. A few abnormal cells seen in the femur of MDA-MB-231 cells-injected mice were not found in MDA-MB-231 cells overexpressing miR-4638. CONCLUSION: The identified functional role of ATF3 targeting miR-4638-3p in BC bone metastasis in vivo suggests its candidature as BC therapeutics in the future.

Linear and Whorled Nevoid Hypermelanosis - A Case of Pigmentary Mosaicism.

Linear and whorled nevoid hypermelanosis is a rare skin pigmentation disorder, characterized by linear streaks and whorls of hyperpigmented macules along Blaschko's lines. Lesions are commonly restricted to the trunk, neck, and extremities, sparing the face, palms, soles, and mucosae. Associated with this, certain cardiovascular, musculoskeletal, neurological, and developmental anomalies have been reported in the literature. Herein, we present a rare case of linear and whorled nevoid hypermelanosis involving the face, with musculoskeletal, genital, aural, and ocular abnormalities.

MicroRNAs mediated interaction of tumor microenvironment cells with breast cancer cells during bone metastasis.

Breast cancer (BC) bone metastasis is primarily osteolytic and has limited therapeutic options. Metastasized BC cells prime the secondary environment in bone by forming a tumor niche, which favors their homing and colonization. The tumor microenvironment (TME) is primarily generated by the cancer cells. Bone TME is an intricate network of multiple cells, including altered bone, tumor, stromal, and immune cells. Recent findings highlight the significance of small non-coding microRNAs (miRNAs) in influencing TME during tumor metastasis. MiRNAs from TME-resident cells facilitate the interaction between the tumor and its microenvironment, thereby regulating the biological processes of tumors. These miRNAs can serve as oncogenes or tumor suppressors. Hence, both miRNA inhibitors and mimics are extensively utilized in pre-clinical trials for modulating the phenotypes of tumor cells and associated stromal cells. This review briefly summarizes the recent developments on the functional role of miRNAs secreted directly or indirectly from the TME-resident cells in facilitating tumor growth, progression, and metastasis. This information would be beneficial in developing novel targeted therapies for BC.

Circ_CUX1/miR-130b-5p/p300 axis for parathyroid hormone-stimulation of Runx2 activity in rat osteoblasts: A combined bioinformatic and experimental approach.

Parathyroid hormone (PTH) regulates the expression of bone remodeling genes by enhancing the activity of Runx2 in osteoblasts. p300, a histone acetyltransferase, acetylated Runx2 to activate the expression of its target genes. PTH stimulated the expression of p300 in rat osteoblastic cells. Increasing studies suggested the potential of non-coding RNAs (ncRNAs), such as microRNAs (miRNAs) and circular RNAs (circRNAs), in regulating gene expression under both physiological and pathological conditions. In this study, we hypothesized that PTH regulates Runx2 activity via ncRNAs-mediated p300 expression in rat osteoblastic cells. Bioinformatics and experimental approaches identified PTH-upregulation of miR-130b-5p and circ_CUX1 that putatively target p300 and miR-130b-5p, respectively. An antisense-mediated knockdown of circ_CUX1 was performed to determine the sponging activity of circ_CUX1. Knockdown of circ_CUX1 promoted miR-130b-5p activity and reduced p300 expression, resulting in decreased Runx2 acetylation in rat osteoblastic cells. Further, bioinformatics analysis identified the possible signaling pathways that regulate Runx2 activity and osteoblast differentiation via circ_CUX1/miR-130b-5p/p300 axis. The predicted circ_CUX1/miR-130b-5p/p300 axis might pave the way for better diagnostic and therapeutic approaches for bone-related diseases.

Regulation of Wnt signaling by non-coding RNAs during osteoblast differentiation.

Bone is a rigid, mineralized connective tissue that constitutes part of the skeleton in most vertebrate animals. Bone remodeling is a complex process that involves the coordination of ossification and bone resorption activities by osteoblasts and osteoclasts, respectively, resulting in maintaining bone mass. This process involves several growth factors/cytokines and hormones regulating the various signaling pathways. Wnt is one of the major molecular signaling pathways that positively regulate the osteogenic differentiation of mesenchymal stem cells. Dysregulation in the Wnt signaling leads to serious bone-related disorders like osteoporosis and osteosclerosis. Recently, several studies reported the critical role of non-coding RNAs (ncRNAs), including microRNAs, long ncRNAs, and circular RNAs, in the regulation of bone homeostasis via modulating the Wnt signaling cascade. This review summarizes the importance of such ncRNAs in mediating the Wnt cascade and its effect on osteoblast differentiation. Understanding the regulatory role of these ncRNAs would serve as a novel therapeutic strategy for treating bone-related disorders.

MiR-4638-3p regulates transforming growth factor-ß1-induced activating transcription factor-3 and cell proliferation, invasion, and apoptosis in human breast cancer cells.

TGF-ß1 (transforming growth factor-beta1), a secreted polypeptide cytokine, stimulates ATF-3 (activating transcription factor-3) expression in a sustained and prolonged manner in human breast cancer cells (MDA-MB231), but not in normal human mammary epithelial cells (MCF-10A). Cyclin A (cell proliferation gene), Runx2 (metastasis gene), and MMP-13 (matrix metalloproteinase-13; invasive gene) were identified as ATF-3 target genes in these cells. Because ATF-3 has very few druggable sites, its direct targeting is difficult. Recent evidence has indicated that microRNAs (miRNAs) are key players in the post-transcriptional modulation of gene expression under several conditions. Bioinformatic analysis suggested a list of putative miRNAs that target ATF-3. Therefore, we hypothesized that TGF-ß1 downregulates the miRNAs that target ATF-3, resulting in the activation of genes that participate in breast cancer progression and skeletal metastasis. Our findings indicate that TGF-ß1 downregulated the expression of miR-4638-3p in MDA-MB231 cells. At the molecular level, forced expression of miR-4638-3p reduced the expression of ATF-3 and its downstream targets, Runx2 and MMP-13, in these cells. At the cellular level, overexpression of miR-4638-3p reduced proliferation, invasion, and migration, and induced G0/G1 cell cycle arrest and apoptosis in MDA-MB231 cells. Overall, this study highlights the possibility of utilizing miR-4638-3p as a therapeutic molecule to curb skeletal metastasis of breast cancer cells.

Exosomes in bone remodeling and breast cancer bone metastasis.

Exosomes are endosome-derived microvesicles that carry cell-specific biological cargo, such as proteins, lipids, and noncoding RNAs (ncRNAs). They play a key role in bone remodeling by enabling the maintenance of a balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption. Recent evidence indicates that exosomes disrupt bone remodeling that occurs during breast cancer (BC) progression. The bone is a preferred site for BC metastasis owing to its abundant osseous reserves. In this review, we aimed to highlight the roles of exosomes derived from bone cells and breast tumor in bone remodeling and BC bone metastasis (BCBM). We also briefly outline the mechanisms of action of ncRNAs and proteins carried by exosomes secreted by bone and BCBM. Furthermore, this review highlights the potential of utilizing exosomes as biomarkers or delivery vehicles for the diagnosis and treatment of BCBM.

Role of p300, a histone acetyltransferase enzyme, in osteoblast differentiation.

Bone is a dynamic and tough connective tissue that undergoes constant remodeling throughout life. Bone-forming osteoblasts respond to various hormones, cytokines, and growth factors, and synthesize extracellular matrix components. Runx2 (Runt-related transcription factor 2), a bone transcription factor, is essential for ossification by stimulating the expression of osteoblast differentiation marker genes, including type I collagen, alkaline phosphatase, and osteocalcin. Coactivators, such as p300, CBP (CREB-binding protein), and PCAF (p300/CBP associated factor) tightly regulate osteoblast differentiation via Runx2. There is growing evidence indicating the role of p300, which possesses histone acetyltransferase (HAT) activity, in regulating histones and transcription factors such as Runx2 during osteoblast differentiation. In this review, we aim to delineate the role of p300 at the molecular level, emphasizing the importance of its HAT activity during osteoblast differentiation. Furthermore, this review intends to highlight the regulation of p300 at multiple levels, including post-translational and ncRNAs, that might exert an indirect influence on bone formation.

A regulatory role of circRNA-miRNA-mRNA network in osteoblast differentiation.

Osteoblast differentiation is an important process in skeletal development and bone remodelling. Serious bone diseases occur from any delay, defect, or imbalance in osteoblastic differentiation. Non-coding RNAs (ncRNAs) play a regulatory role in controlling the expression of proteins under physiological and pathological conditions via inhibiting mRNA translation or degrading mRNA. Circular RNAs (circRNAs) and microRNAs (miRNAs) are the long and small ncRNAs, respectively, which have been reported to regulate the expression of osteoblast marker genes directly or indirectly. Also, recent studies identified the regulatory mechanisms involving the crosstalk among circRNAs, miRNAs, and mRNAs during osteoblast differentiation. Understanding these regulatory mechanisms behind osteoblastic differentiation would help to diagnose or treat bone and bone-related disorders. Hence, the current review comprehensively discussed the regulatory relationship of circRNAs, miRNAs and mRNAs, and their functional role as circRNA-miRNA-mRNA axis in osteoblast differentiation.

Hospital-Based Contact Tracing of Patients With COVID-19 and Health Care Workers During the COVID-19 Pandemic in Eastern India: Cross-sectional Study.

BACKGROUND: The contact tracing and subsequent quarantining of health care workers (HCWs) are essential to minimizing the further transmission of SARS-CoV-2 infection and mitigating the shortage of HCWs during the COVID-19 pandemic situation. OBJECTIVE: This study aimed to assess the yield of contact tracing for COVID-19 cases and the risk stratification of HCWs who are exposed to these cases. METHODS: This was an analysis of routine data that were collected for the contact tracing of COVID-19 cases at the All India Institute of Medical Sciences, Bhubaneswar, in Odisha, India. Data from March 19 to August 31, 2020, were considered for this study. COVID-19 cases were admitted patients, outpatients, or HCWs in the hospital. HCWs who were exposed to COVID-19 cases were categorized, per the risk stratification guidelines, as high-risk contacts or low-risk contacts. RESULTS: During contact tracing, 3411 HCWs were identified as those who were exposed to 360 COVID-19 cases. Of these 360 cases, 269 (74.7%) were either admitted patients or outpatients, and 91 (25.3%) were HCWs. After the risk stratification of the 3411 HCWs, 890 (26.1%) were categorized as high-risk contacts, and 2521 (73.9%) were categorized as low-risk contacts. The COVID-19 test positivity rates of high-risk contacts and low-risk contacts were 3.8% (34/890) and 1.9% (48/2521), respectively. The average number of high-risk contacts was significantly higher when the COVID-19 case was an admitted patient (number of contacts: mean 6.6) rather than when the COVID-19 case was an HCW (number of contacts: mean 4.0) or outpatient (number of contacts: mean 0.2; P=.009). Similarly, the average number of high-risk contacts was higher when the COVID-19 case was admitted in a non-COVID-19 area (number of contacts: mean 15.8) rather than when such cases were admitted in a COVID-19 area (number of contacts: mean 0.27; P<.001). There was a significant decline in the mean number of high-risk contacts over the study period (P=.003). CONCLUSIONS: Contact tracing and risk stratification were effective and helped to reduce the number of HCWs requiring quarantine. There was also a decline in the number of high-risk contacts during the study period. This indicates the role of the implementation of hospital-based, COVID-19-related infection control strategies. The contact tracing and risk stratification approaches that were designed in this study can also be implemented in other health care settings.

A computational approach on studying the regulation of TGF-ß1-stimulated Runx2 expression by MicroRNAs in human breast cancer cells.

BACKGROUND: Transforming growth factor-beta1 (TGF-ß1) acts as a most effective growth inhibitor for normal epithelial cells. Loss of this anti-proliferative factor in breast tissues favors invasion and development of osteolytic metastases, aided by a master transcription factor, runt-related transcription factor 2 (Runx2). Several reports identified Runx2 regulation with the help of non-coding RNAs such as microRNAs (miRNAs) under physiological and pathological conditions. METHODS: Using bioinformatics tools such as miRDB, STarMir, Venny, TarBase, a unique list of miRNAs that putatively target the 3' UTR Runx2 was identified. Further, the expression patterns of those miRNAs at the precursor and mature levels were studied by RT-qPCR analyses. Following this, computational analyses using software like TransmiR and bc-GenExMiner v4.6 were done to speculate the miRNA's other target genes that indirectly regulate Runx2 activity in breast cancer. RESULTS: There were 13 miRNAs that putatively target Runx2 identified using bioinformatics tools. Among these miRNAs, miR-5703 expression was significantly downregulated at both precursor and mature levels upon TGF-ß1-treatment in human breast cancer cells. Computational analyses speculated an indirect targeting of Runx2 by miR-5703 by influencing multiple Runx2 regulatory signaling pathways including Jak/Stat, MAPK, Wnt/ß-Catenin, Notch, BMP, and PKA pathways. Furthermore, a correlation of the expression profiles of the speculated genes and Runx2 with miR-5703 was depicted in triple-negative breast cancer patients. CONCLUSION: Identification of miR-5703 and its network for Runx2 regulation directly or indirectly in breast cancer cells could significantly advance our understanding of breast cancer-mediated bone metastasis. In addition, it would potentially pave the way for miRNAs to be used as biomarkers and therapeutic agents in cancer research.

Regulation of bone metastasis and metastasis suppressors by non-coding RNAs in breast cancer.

Breast cancer (BC) is a critical health care issue that substantially affects women worldwide. Though surgery and chemotherapy can effectively control tumor growth, metastasis remains a primary concern. Metastatic BC cells predominantly colonize in bone, owing to their rigid osseous nutrient-rich nature. There are recently increasing studies investigating the context-dependent roles of non-coding RNAs (ncRNAs) in metastasis regulation. ncRNAs, including microRNAs, long non-coding RNAs, circular RNAs, and small interference RNAs, control the BC metastasis via altered mechanisms. Additionally, these ncRNAs have been reported in regulating a unique class of genes known as Metastatic suppressors. Metastasis suppressors like BRMS1, NM23, LIFR, and KAI1, etc., have been extensively studied for their role in inducing apoptosis, inhibiting metastasis, and maintaining homeostasis. In this review, we have emphasized the direct regulation of ncRNAs for effectively controlling the distant spread of BC. Furthermore, we have highlighted the ncRNA-mediated modulation of the metastatic suppressors, thereby delineating their indirect influence over metastasis.

A computational study of non-coding RNAs on the regulation of activating transcription factor 3 in human breast cancer cells.

We previously reported that activating transcription factor 3 (ATF3), an adaptive response gene, plays a dichotomous role in regulating several molecular processes during breast cancer progression. ATF3 promoted the expression of runt-related transcription factor 2 (Runx2, a metastatic gene) and activated matrix metalloproteinase 13 (MMP13, an invasive gene), thereby fostering proliferation and bone-metastasis of the breast cancer cells. Targeting ATF3 may mitigate the metastatic spread of breast cancer and improve the patient's lifespan. Non-coding RNAs (ncRNAs) such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) are the new-era regimens that are currently utilized for diagnosis and treatment of a variety of malignancies including cancer. mir-3674 putatively targets ATF3, but its expression was significantly increased in human breast cancer cells (MDA-MB231), compared to normal human mammary epithelial cells (MCF-10A). Our in silico analysis identified a few lncRNAs and circRNAs showing their putative binding sites for miR-3674. Thus, mir-3674, despite its abundance in the MDA-MB231 cells, could not effectively target ATF3, which could be due to the sponging mechanism of lncRNAs and circRNAs towards mir-3674. More extensive in vitro and in vivo studies are required to validate this and expand the diagnostic and therapeutic perspectives of breast cancer.

Association of HOTAIR (rs920778 and rs1899663) and NME1 (rs16949649 and rs2302254) gene polymorphisms with breast cancer risk in India.

BACKGROUND: Until now, no study has reported the combined effect of genetic variants of HOTAIR and NME1 towards breast cancer (BC) pathogenesis. Hence, the aim of the present study is to determine the risk of breast cancer development with HOTAIR (rs920778 C > T and rs1899663 G > T) and NME1 (rs16949649 T > C and rs2302254 C > T) genetic polymorphisms in the Indian population for the first time. MATERIALS AND METHODS: To investigate the genetic association of these four SNPs, we conducted a population-based case-control study involving 1011 subjects (502 histologically confirmed BC patients and 509 disease-free controls) using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. RESULTS: HOTAIR rs920778 TC genotype elevated the risk of BC (OR = 1.39, 95% CI = 1.06-1.83, p = 0.018) and individuals carrying the mutant allele (T) of rs1899663 had increased BC risk (OR = 1.23, 95% CI = 1.02-1.47, p = 0.026). The presence of the NME1 rs16949649 CC genotype increased the risk of BC (OR = 1.76, 95% CI = 1.15-2.71, p = 0.009). Moreover, the HOTAIR rs920778 variant (TC + CC) increased the risk of BC in pre-menopausal women (OR = 5.86; p < 0.0001). Women carrying 2 or 3 mutant alleles for the investigated SNPs were observed to have an elevated risk of BC. CONCLUSION: The results of the present study highlight the presence of significant associations between NME1 rs16949649 and HOTAIR (rs920778 and rs1899663) polymorphisms and breast cancer development in Indian women.

An osteoinductive effect of phytol on mouse mesenchymal stem cells (C3H10T1/2) towards osteoblasts.

In recent years, phytochemicals have been widely researched and utilized for the treatment of various medical conditions such as cancer, cardiovascular diseases, age-related problems and are also said to have bone regenerative effects. In this study, phytol (3,7,11,15-tetramethylhexadec-2-en-1-ol), an acyclic unsaturated diterpene alcohol and a secondary metabolite derived from aromatic plants was investigated for its effect on osteogenesis. Phytol was found to be nontoxic in mouse mesenchymal stem cells (C3H10T1/2). At the cellular level, phytol-treatment promoted osteoblast differentiation, as seen by the increased calcium deposits. At the molecular level, phytol-treatment stimulated the expression of Runx2 (a bone-related transcription factor) and other osteogenic marker genes. MicroRNAs (miRNAs) play an essential role in controlling bone metabolism by targeting genes at the post-transcriptional level. Upon phytol-treatment in C3H10T1/2 cells, mir-21a and Smad7 levels were increased and decreased, respectively. It was previously reported that mir-21a targets Smad7 (an antagonist of TGF-beta1 signaling) and thus, protects Runx2 from its degradation. Thus, based on our results, we suggest that phytol-treatment promoted osteoblast differentiation in C3H10T1/2 cells via Runx2 due to downregulation of Smad7 by mir-21a. Henceforth, phytol was identified to bolster osteoblast differentiation, which in turn may be used for bone regeneration.

HOTAIR LncRNA: A novel oncogenic propellant in human cancer.

Long non-coding RNAs (lncRNAs) are an important novel class of non-coding RNAs having lengths of 200 nucleotides and low expression. The HOX Transcript Antisense Intergenic RNA (HOTAIR) is one of the most extensively studied lncRNAs found dysregulated in human cancer. Although a growing body of evidence suggests a role fo HOTAIR in pathogenesis, disease progression, drug resistance and reduced survival, its mechanism of action remains largely unclear. Recent studies have identified that HOTAIR facilitates protein-protein interaction thereby affecting diverse pathways in cancer such as epigenetic reprogramming, protein stability and signal transduction. HOTAIR has been shown to promote tumor progression by regulating microRNA expression and function. Moreover, several HOTAIR gene variants have recently been identified and found to increase cancer susceptibility. Here we review recent data on the critical role of HOTAIR in human malignancy and its potential mechanism of action. A more comprehensive understanding of this unique lncRNA is critical to elucidating the pro-oncogenic function of HOTAIR its potential application in diagnosis, prognosis and treatment.

A logical and sustainable approach towards bamboo pulp bleaching using xylanase from Aspergillus nidulans.

Driven by the environmental benefits that bio-bleaching could bring, the interest in xylanase has received enormous attention and hence, the search of xylanase with properties like no cellulase activity, function at elevated temperatures and pH continues. The present study reports the production of extracellular xylanase from Aspergillus nidulans using waste agro-residues as substrate. The optimum temperature (60 °C) and pH (9.0), classified the xylanase as thermo and alkali tolerant. The addition of salt of Mn2+ increased the xylanase activity to almost double; however, these ions were unable to protect the enzyme from thermal inactivation. The FTIR spectra of bamboo pulp treated with this xylanase, revealed reduction in lignin as evident from reduced peak intensity coupled with the reduction in kappa number. The SEM image of enzyme treated pulp, exhibited dissociation in fibers exposing the internal structure with slight roughness. Swelling was also observed there by increasing its thickness which eventually helped in improving its physical properties. The bleaching efficacy of indigenous xylanase as indicated in this study, has established its competence as a promising candidate for pre-treating the bamboo pulp.

Preparation, characterization and in vitro evaluation of tablets containing microwave-assisted solid dispersions of apremilast.

BACKGROUND: Solid dispersions are among the techniques successfully employed to enhance the dissolution of poorly water-soluble drugs. Microwave (MW)-assisted evaporative crystallization has been used to prepare solid dispersions of drugs and polymers. OBJECTIVES: The aim of the study was to investigate the solubility of apremilast (APM) in water by exploring the effect of MW-assisted solid dispersion technology. MATERIAL AND METHODS: In the present study, solid dispersions of APM, a poorly water-soluble drug, were prepared. The solid dispersions were prepared using the conventional method (CM) and the MW-based solvent evaporation technique. Microwave energy was used to enhance the solubility and dissolution rate of APM. The physical mixture and solid dispersions were characterized using Fourier-transform infrared spectroscopy (FTIR), X-ray powder diffraction (XRPD), differential scanning calorimetry (DSC), and scanning electron microscopy (SEM). Apremilast tablets containing MW-assisted solid dispersions were prepared by the direct compression technique and compared with the marketed formulation (Aprezo tablets). RESULTS: The results obtained confirmed the conversion of crystalline APM to an amorphous form. The XRPD pattern of the MW-assisted formulation at a 2:1 ratio suggests the amorphous structure of APM within the formulation. Based on solubility studies results, Syloid® 244FP was selected as the best carrier. The dissolution study results suggested that the APM tablet prepared using MW-assisted solid dispersions at a 2:1 carrier/drug ratio improved the APM dissolution rate compared to the marketed formulation. CONCLUSIONS: Based on the results, it can be concluded that the MW-assisted solid dispersion technique may be an effective approach to enhancing the dissolution profile of other poorly water-soluble drugs.