Evidence map›Paper›PMID 42387613›Full record

ArticleStem cell research & therapy2026

Emerging roles of the long non-coding RNAs MALAT1 and TUG1 during differentiation of adipose tissue-derived mesenchymal stem cells towards insulin-producing cells.

Eman F Sanad, Alaa Ahmed Saad, Joy Rafeek, Rana Mokbel, Mayar Abdallah, Nadeen Emad, Hagar Adel Mohamed, Yasmin Alaa, Yumna Medhat Mahmoud, Dina H Kassem

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Article in Stem cell research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

10 authors.

Eman F SanadDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt.
Alaa Ahmed SaadDrug Design Program, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt.
Joy RafeekDrug Design Program, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt.
Rana MokbelDrug Design Program, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt.
Mayar AbdallahDrug Design Program, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt.
Nadeen EmadDrug Design Program, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt.
Hagar Adel MohamedDrug Design Program, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt.
Yasmin AlaaDrug Design Program, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt.
Yumna Medhat MahmoudDrug Design Program, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt.
Dina H KassemDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt. dina_kassem@pharma.asu.edu.eg.ORCID http://orcid.org/0000-0001-5102-3235

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGeneration of insulin-producing cells (IPCs) from stem cells provides great hope for patients with diabetes mellitus (DM). Long non-coding RNAs (lncRNAs) ignited much interest regarding their role in determining the fate of stem cells. The lncRNAs MALAT1 and TUG1 have been reported to be interrelated with β-cell dysfunction and/or DM. However, their role during generation of IPCs from stem cells has not been adequately studied. Thus, the current study aimed to investigate the role of MALAT1 and TUG1 during differentiation of adipose tissue-derived mesenchymal stem cells (Ad-MSCs) towards IPCs.

methodsAd-MSCs were isolated from rat epididymal fat pads, characterized and induced to differentiate towards IPCs. Assessment of differentiation was done by measuring expression levels of various β-cell-related markers using RT-qPCR, as well as morphological changes, and dithizone staining. Expression levels of MALAT1 and TUG1 were also measured by RT-qPCR. Several in-silico analyses were done using RNA-protein Association and Interaction Networks (RAIN) database.

resultsMALAT1 and TUG1 expression levels were significantly increased during differentiation of Ad-MSCs into IPCs as compared to control uninduced cells. Furthermore, generated networks from RAIN database revealed an interplay between MALAT1 and TUG1, and between each of them with several common targets like GAS5, HOTAIR and TP53COR1.

conclusionsThe current study portrays MALAT1 and TUG1 as novel interrelated molecular mediators and important regulatory nodes enhancing differentiation of Ad-MSCs towards IPCs. Their upregulation during differentiation can be interrelated with competitive endogenous RNA (ceRNA) networks, mediating various epigenetic modifications, orchestrating signaling pathways and overcoming cellular stress during reprogramming/differentiation.

Indexed as

Adipose TissueCell DifferentiationInsulin-Secreting CellsMesenchymal Stem CellsRNA, Long NoncodingAnimalsInsulinMaleRatsInsulinMALAT1 long noncoding RNA, ratRNA, Long NoncodingTUG1 long noncoding RNA, ratDiabetes mellitusDifferentiationInsulin-producing cellsLong non-coding RNAsMesenchymal stem cells

Identifiers

PMID42387613
PMCPMC13325589

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