SNHG10 promote tumorigenesis via miR-150/VEGFA/EGFR/AKT/ERK/mTOR axis and gemcitabine resistance in PDAC Article Swipe
Gouri Pandya
,
Aishwarya Singh
,
Suman Sourav
,
Sharon Raju
,
Rachana Kumari
,
Rashi Sharma
,
Vishakha Goyal
,
Bhudev C. Das
,
Gautam Sethi
,
Amit Kumar Pandey
,
Deepti Pandita
,
Rajender K. Motiani
,
Manoj Garg
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1101/2025.04.24.650424
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1101/2025.04.24.650424
SNHG10 emerged as a key regulator in progression and metastasis of cancers. However, potential of SNHG10 in PDAC tumorigenesis, gemcitabine resistance, and underlying mechanisms remains poorly understood. We observed significant upregulation of SNHG10 in 179 PDAC cases, revealing a positive correlation with clinical stages. Our results showed a significant SNHG10 overexpression in several PDAC cells. Downregulation of SNHG10 significantly decreased the proliferation, clonogenicity, EMT, tumor growth in the xenograft model, and the induction of cell cycle arrest and apoptosis of PDAC cells. Mechanistically, SNHG10 knockdown significantly inhibited the expression of vimentin, N-cadherin, survivin, CDK4, CDK6, cyclin B1, cyclin D1, aurora kinase A, and B, with an increased expression of E-cadherin and p21. RNA Immunoprecipitation data displayed physical interaction among SNHG10, miR-150-5p, and VEGFA in PDAC cells. SNHG10 silencing led to the significant induction of miR-150-5p, which repressed VEGFA expression in PDAC cells. SNHG10 downregulation enhanced gemcitabine sensitivity in PDAC cells. SNHG10 silencing suppressed the phosphorylation of EGFR, AKT, ERK1/2, mTOR, and c-MET pathways. Silencing SNHG10 and its regulated signalling offers a novel prospective therapeutic strategy.
Related Topics
Concepts
Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1101/2025.04.24.650424
- https://www.biorxiv.org/content/biorxiv/early/2025/04/26/2025.04.24.650424.full.pdf
- OA Status
- green
- References
- 62
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4409839958
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4409839958Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1101/2025.04.24.650424Digital Object Identifier
- Title
-
SNHG10 promote tumorigenesis via miR-150/VEGFA/EGFR/AKT/ERK/mTOR axis and gemcitabine resistance in PDACWork title
- Type
-
preprintOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2025Year of publication
- Publication date
-
2025-04-26Full publication date if available
- Authors
-
Gouri Pandya, Aishwarya Singh, Suman Sourav, Sharon Raju, Rachana Kumari, Rashi Sharma, Vishakha Goyal, Bhudev C. Das, Gautam Sethi, Amit Kumar Pandey, Deepti Pandita, Rajender K. Motiani, Manoj GargList of authors in order
- Landing page
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https://doi.org/10.1101/2025.04.24.650424Publisher landing page
- PDF URL
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https://www.biorxiv.org/content/biorxiv/early/2025/04/26/2025.04.24.650424.full.pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
greenOpen access status per OpenAlex
- OA URL
-
https://www.biorxiv.org/content/biorxiv/early/2025/04/26/2025.04.24.650424.full.pdfDirect OA link when available
- Concepts
-
Gemcitabine, PI3K/AKT/mTOR pathway, Protein kinase B, MAPK/ERK pathway, Carcinogenesis, Cancer research, Chemistry, Medicine, Internal medicine, Signal transduction, Cancer, BiochemistryTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
- References (count)
-
62Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.B, | 104 |
| abstract_inverted_index.We | 28 |
| abstract_inverted_index.an | 106 |
| abstract_inverted_index.as | 3 |
| abstract_inverted_index.in | 7, 17, 34, 52, 67, 124, 140, 148 |
| abstract_inverted_index.of | 11, 15, 32, 57, 74, 80, 90, 109, 134, 156 |
| abstract_inverted_index.to | 130 |
| abstract_inverted_index.179 | 35 |
| abstract_inverted_index.B1, | 97 |
| abstract_inverted_index.D1, | 99 |
| abstract_inverted_index.Our | 45 |
| abstract_inverted_index.RNA | 113 |
| abstract_inverted_index.and | 9, 22, 71, 78, 103, 111, 122, 161, 166 |
| abstract_inverted_index.its | 167 |
| abstract_inverted_index.key | 5 |
| abstract_inverted_index.led | 129 |
| abstract_inverted_index.the | 61, 68, 72, 88, 131, 154 |
| abstract_inverted_index.AKT, | 158 |
| abstract_inverted_index.EMT, | 64 |
| abstract_inverted_index.PDAC | 18, 36, 54, 81, 125, 141, 149 |
| abstract_inverted_index.cell | 75 |
| abstract_inverted_index.data | 115 |
| abstract_inverted_index.p21. | 112 |
| abstract_inverted_index.with | 42, 105 |
| abstract_inverted_index.CDK4, | 94 |
| abstract_inverted_index.CDK6, | 95 |
| abstract_inverted_index.EGFR, | 157 |
| abstract_inverted_index.VEGFA | 123, 138 |
| abstract_inverted_index.among | 119 |
| abstract_inverted_index.c-MET | 162 |
| abstract_inverted_index.cycle | 76 |
| abstract_inverted_index.mTOR, | 160 |
| abstract_inverted_index.novel | 172 |
| abstract_inverted_index.tumor | 65 |
| abstract_inverted_index.which | 136 |
| abstract_inverted_index.SNHG10 | 1, 16, 33, 50, 58, 84, 127, 143, 151, 165 |
| abstract_inverted_index.arrest | 77 |
| abstract_inverted_index.aurora | 100 |
| abstract_inverted_index.cases, | 37 |
| abstract_inverted_index.cells. | 55, 82, 126, 142, 150 |
| abstract_inverted_index.cyclin | 96, 98 |
| abstract_inverted_index.growth | 66 |
| abstract_inverted_index.kinase | 101 |
| abstract_inverted_index.model, | 70 |
| abstract_inverted_index.offers | 170 |
| abstract_inverted_index.poorly | 26 |
| abstract_inverted_index.showed | 47 |
| abstract_inverted_index.ERK1/2, | 159 |
| abstract_inverted_index.SNHG10, | 120 |
| abstract_inverted_index.emerged | 2 |
| abstract_inverted_index.remains | 25 |
| abstract_inverted_index.results | 46 |
| abstract_inverted_index.several | 53 |
| abstract_inverted_index.stages. | 44 |
| abstract_inverted_index.Abstract | 0 |
| abstract_inverted_index.However, | 13 |
| abstract_inverted_index.cancers. | 12 |
| abstract_inverted_index.clinical | 43 |
| abstract_inverted_index.enhanced | 145 |
| abstract_inverted_index.observed | 29 |
| abstract_inverted_index.physical | 117 |
| abstract_inverted_index.positive | 40 |
| abstract_inverted_index.Silencing | 164 |
| abstract_inverted_index.apoptosis | 79 |
| abstract_inverted_index.decreased | 60 |
| abstract_inverted_index.displayed | 116 |
| abstract_inverted_index.increased | 107 |
| abstract_inverted_index.induction | 73, 133 |
| abstract_inverted_index.inhibited | 87 |
| abstract_inverted_index.knockdown | 85 |
| abstract_inverted_index.pathways. | 163 |
| abstract_inverted_index.potential | 14 |
| abstract_inverted_index.regulated | 168 |
| abstract_inverted_index.regulator | 6 |
| abstract_inverted_index.repressed | 137 |
| abstract_inverted_index.revealing | 38 |
| abstract_inverted_index.silencing | 128, 152 |
| abstract_inverted_index.strategy. | 175 |
| abstract_inverted_index.survivin, | 93 |
| abstract_inverted_index.vimentin, | 91 |
| abstract_inverted_index.xenograft | 69 |
| abstract_inverted_index.E-cadherin | 110 |
| abstract_inverted_index.expression | 89, 108, 139 |
| abstract_inverted_index.mechanisms | 24 |
| abstract_inverted_index.metastasis | 10 |
| abstract_inverted_index.signalling | 169 |
| abstract_inverted_index.suppressed | 153 |
| abstract_inverted_index.underlying | 23 |
| abstract_inverted_index.N-cadherin, | 92 |
| abstract_inverted_index.correlation | 41 |
| abstract_inverted_index.gemcitabine | 20, 146 |
| abstract_inverted_index.interaction | 118 |
| abstract_inverted_index.miR-150-5p, | 121, 135 |
| abstract_inverted_index.progression | 8 |
| abstract_inverted_index.prospective | 173 |
| abstract_inverted_index.resistance, | 21 |
| abstract_inverted_index.sensitivity | 147 |
| abstract_inverted_index.significant | 30, 49, 132 |
| abstract_inverted_index.therapeutic | 174 |
| abstract_inverted_index.understood. | 27 |
| abstract_inverted_index.upregulation | 31 |
| abstract_inverted_index.significantly | 59, 86 |
| abstract_inverted_index.Downregulation | 56 |
| abstract_inverted_index.clonogenicity, | 63 |
| abstract_inverted_index.downregulation | 144 |
| abstract_inverted_index.overexpression | 51 |
| abstract_inverted_index.proliferation, | 62 |
| abstract_inverted_index.tumorigenesis, | 19 |
| abstract_inverted_index.phosphorylation | 155 |
| abstract_inverted_index.Mechanistically, | 83 |
| abstract_inverted_index.Immunoprecipitation | 114 |
| cited_by_percentile_year | |
| countries_distinct_count | 0 |
| institutions_distinct_count | 13 |
| citation_normalized_percentile.value | 0.14193489 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |