---
title: "PIP4K2A depletion reduces AKT signaling and increases chemotherapy sensitivity in T‑cell lymphobla"
id: "pubmed-42570494"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42570494"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42570494/"
doi: "10.1016/j.bbrc.2026.154404"
published_at: "2026-09-24T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# PIP4K2A depletion reduces AKT signaling and increases chemotherapy sensitivity in T‑cell lymphobla
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42570494
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42570494/)
- **DOI:** [10.1016/j.bbrc.2026.154404](https://doi.org/10.1016%2Fj.bbrc.2026.154404)
- **Published At:** 2026-09-24T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- T-cell lymphoblastic lymphoma (T-LBL) is an aggressive immature T-cell malignancy with frequent activation of pro-survival pathways including **PI3K/AKT/mTORC1**. - The study used the human T-LBL cell line Sup-T1 to test effects of reducing PIP4K family members on signaling, proliferation, and drug response. - Doxycycline-inducible shRNA knockdown of **PIP4K2A** and **PIP4K2B** reduced Sup-T1 proliferation and increased sensitivity to multiple chemotherapeutic agents. - Knockdown of **PIP4K2A** alone reproduced most of the enhanced chemosensitivity seen with combined PIP4K2A/2B depletion; PIP4K2B knockdown had a smaller effect. - PIP4K2A knockdown markedly decreased AKT phosphorylation, whereas PIP4K2B depletion produced a smaller reduction. - Combined depletion of PIP4K2A/2B caused a pronounced decrease in S6K phosphorylation, indicating reduced **mTORC1** activity; single knockdowns produced only modest changes in S6K phosphorylation. - Two structurally distinct small-molecule PIP4K2A inhibitors (066ATZ and BAY-091) did not reduce Sup-T1 proliferation, alter nelarabine sensitivity, or diminish AKT phosphorylation. - The lack of effect from kinase inhibitors suggests PIP4K2A may support AKT signaling through a **non-catalytic** mechanism in these cells. - Findings identify PIP4K2A as a positive regulator of AKT signaling and a determinant of chemotherapy sensitivity in Sup-T1 T-LBL cells and motivate further study of its non-enzymatic roles in therapy response.
## Clinical Analysis & Structured Key Points
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Epub 2026 Aug 7. # PIP4K2A depletion suppresses AKT signaling and enhances chemotherapy sensitivity in T-cell lymphoblastic lymphoma cells [Song Chen](https://pubmed.ncbi.nlm.nih.gov/?term=Chen+S&cauthor_id=42570494)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42570494/#full-view-affiliation-1 "Department of Pharmacology, Yale School of Medicine, New Haven, CT, 06520, USA."), [Zunyu He](https://pubmed.ncbi.nlm.nih.gov/?term=He+Z&cauthor_id=42570494)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42570494/#full-view-affiliation-1 "Department of Pharmacology, Yale School of Medicine, New Haven, CT, 06520, USA."), [Ya Ha](https://pubmed.ncbi.nlm.nih.gov/?term=Ha+Y&cauthor_id=42570494)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42570494/#full-view-affiliation-2 "Department of Pharmacology, Yale School of Medicine, New Haven, CT, 06520, USA. Electronic address: ya.ha@yale.edu.") Affiliations Expand ### Affiliations * 1 Department of Pharmacology, Yale School of Medicine, New Haven, CT, 06520, USA. * 2 Department of Pharmacology, Yale School of Medicine, New Haven, CT, 06520, USA. Electronic address: ya.ha@yale.edu. * PMID: **42570494** * PMCID: [ PMC13528604 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13528604/) * DOI: [ 10.1016/j.bbrc.2026.154404 ](https://doi.org/10.1016/j.bbrc.2026.154404) Item in Clipboard # PIP4K2A depletion suppresses AKT signaling and enhances chemotherapy sensitivity in T-cell lymphoblastic lymphoma cells Song Chen et al. Biochem Biophys Res Commun. 2026. Show details Display options Display options Format Abstract PubMed PMID Biochem Biophys Res Commun Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Biochem+Biophys+Res+Commun%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Biochem+Biophys+Res+Commun%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42570494/) . 2026 Sep 24:832:154404. doi: 10.1016/j.bbrc.2026.154404. Epub 2026 Aug 7. ### Authors [Song Chen](https://pubmed.ncbi.nlm.nih.gov/?term=Chen+S&cauthor_id=42570494)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42570494/#short-view-affiliation-1 "Department of Pharmacology, Yale School of Medicine, New Haven, CT, 06520, USA."), [Zunyu He](https://pubmed.ncbi.nlm.nih.gov/?term=He+Z&cauthor_id=42570494)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42570494/#short-view-affiliation-1 "Department of Pharmacology, Yale School of Medicine, New Haven, CT, 06520, USA."), [Ya Ha](https://pubmed.ncbi.nlm.nih.gov/?term=Ha+Y&cauthor_id=42570494)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42570494/#short-view-affiliation-2 "Department of Pharmacology, Yale School of Medicine, New Haven, CT, 06520, USA. Electronic address: ya.ha@yale.edu.") ### Affiliations * 1 Department of Pharmacology, Yale School of Medicine, New Haven, CT, 06520, USA. * 2 Department of Pharmacology, Yale School of Medicine, New Haven, CT, 06520, USA. Electronic address: ya.ha@yale.edu. * PMID: **42570494** * PMCID: [ PMC13528604 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13528604/) * DOI: [ 10.1016/j.bbrc.2026.154404 ](https://doi.org/10.1016/j.bbrc.2026.154404) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract T-cell lymphoblastic lymphoma (T-LBL) is an aggressive malignancy of immature T cells characterized by rapid proliferation and frequent activation of pro-survival pathways such as PI3K/AKT/mTORC1 signaling. Although multi-agent chemotherapy can induce remission, relapsed disease is often refractory, underscoring the need to identify vulnerabilities that enhance therapeutic response. Previous studies showed that genetic ablation of Pip4k2a and Pip4k2b protects Trp53-null mice from thymic lymphoma, implicating these lipid kinases in T-cell lymphomagenesis. Here, we show that knockdown of PIP4K2A and PIP4K2B reduced AKT signaling, inhibited proliferation, and increased sensitivity to multiple chemotherapeutic agents in Sup-T1 cells, a human T-LBL cell line. PIP4K2A knockdown largely recapitulated the enhanced chemosensitivity observed following combined PIP4K2A/2B depletion, whereas PIP4K2B knockdown had a more limited effect. Unexpectedly, two structurally distinct PIP4K2A inhibitors failed to suppress Sup-T1 proliferation or viability, suggesting that the kinase supports AKT signaling through an activity-independent mechanism. Although individual knockdown of PIP4K2A or PIP4K2B produced only modest effects on S6K phosphorylation, combined depletion markedly reduced mTORC1 activity. Together, these findings identify PIP4K2A as a positive regulator of AKT signaling in T-LBL cells and provide a motivation for further investigating its non-catalytic functions in chemotherapy response. **Keywords:** AKT signaling; Chemotherapy sensitization; PIP4K; T-cell lymphomagenesis; mTORC1. Copyright © 2026 Elsevier Inc. All rights reserved. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declaration of competing interest The authors have no competing interests to declare. ## Figures [ ![Fig. 1.](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc2a/13528604/410825c760e0/nihms-2203602-f0001.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc2a/13528604/7235b1b078ed/nihms-2203602-f0001.webp) ** Fig. 1.. Knockdown of PIP4K2A and PIP4K2B… ** ** Fig. 1.. Knockdown of PIP4K2A and PIP4K2B expression suppresses Sup-T1 cell proliferation and enhances sensitivity… ** **Fig. 1.. Knockdown of PIP4K2A and PIP4K2B expression suppresses Sup-T1 cell proliferation and enhances sensitivity to nelarabine.** **A.** Sup-T1 cells expressing a doxycycline-inducible shRNA targeting PIP4K2A/2B were cultured in the absence (−DOX, black) or presence (+DOX, red) of doxycycline. Cell proliferation was monitored over 96 h and is presented as fold increase in cell number relative to the initial time point. Data are presented as mean ± SEM from three independent experiments. **B.** Sup-T1 cells were treated with increasing concentrations of nelarabine (0–5 μM) in the absence (−DOX, black) or presence (+DOX, red) of doxycycline. Cell proliferation was measured and expressed as a percentage of the control cells in the absence of nelarabine. Data are presented as mean ± SEM (n = 3). **C.** Immunoblot analysis confirming doxycycline-inducible knockdown of PIP4K2A, PIP4K2B, or both in Sup-T1 cells (top panel). Cell proliferation measured after 72 h and expressed as fold increase in cell number relative to the initial time point (bottom panel). Knockdown of PIP4K2A resulted in a greater reduction in proliferation compared with PIP4K2B knockdown, while simultaneous depletion of both kinases produced the strongest inhibitory effect. Data are presented as mean ± SEM (n=3). Statistical significance was determined using Student’s _t_ -test; ***_P_ < 0.0001; n.s., not significant. **D.** Dose–response curves for nelarabine in Sup-T1 cells expressing doxycycline-inducible shRNAs targeting PIP4K2A (left panel) or PIP4K2B (right panel). Cells were treated with increasing concentrations of nelarabine in the absence (−DOX, solid lines) or presence (+DOX, dashed lines) of doxycycline. Cell proliferation was measured and expressed as a percentage of control cells in the absence of nelarabine. Knockdown of PIP4K2A resulted in a marked increase in drug sensitivity, whereas knockdown of PIP4K2B had minimal effect. Data are presented as mean ± SEM (n = 3). **E.** Immunoblot analysis of phosphorylated AKT (pAKT), ACC (pACC), and S6K (pS6K) in Sup-T1 cells following doxycycline-inducible knockdown of PIP4K2A, PIP4K2B, or both. Knockdown of PIP4K2A markedly reduced AKT phosphorylation, whereas PIP4K2B depletion had a smaller effect. Combined knockdown of PIP4K2A/2B reduced S6K phosphorylation, indicative of decreased mTORC1 activity, without a corresponding increase in ACC phosphorylation. [ ![Fig. 2.](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc2a/13528604/0ba4fada00d2/nihms-2203602-f0002.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc2a/13528604/fb2f496f8347/nihms-2203602-f0002.webp) ** Fig. 2.. PIP4K2A/2B depletion broadly enhances sensitivity… ** ** Fig. 2.. PIP4K2A/2B depletion broadly enhances sensitivity of Sup-T1 cells to chemotherapeutic agents. ** Dose–response curves… **Fig. 2.. PIP4K2A/2B depletion broadly enhances sensitivity of Sup-T1 cells to chemotherapeutic agents.** Dose–response curves for a panel of chemotherapeutic agents in Sup-T1 cells expressing a doxycycline-inducible shRNA targeting PIP4K2A/2B. Cells were treated with increasing concentrations of each drug in the absence (−DOX, solid lines) or presence (+DOX, dashed lines) of doxycycline. Cell proliferation was measured and expressed as a percentage of control cells in the absence of drug. **A.** Antimetabolites: cytarabine, methotrexate, and 6-mercaptopurine (6-MP). **B.** DNA-damaging agents: doxorubicin, etoposide, and 4-hydroperoxycyclophosphamide (4-OOH-CP). **C.** Dexamethasone. **D.** _L_ -asparaginase. **E.** Vincristine. Data are presented as mean ± SEM (n = 3). [ ![Fig. 3.](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc2a/13528604/19b7f20d88a3/nihms-2203602-f0003.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc2a/13528604/f37c86a5891c/nihms-2203602-f0003.webp) ** Fig. 3.. PIP4K2A knockdown is primarily responsible… ** ** Fig. 3.. PIP4K2A knockdown is primarily responsible for enhanced cytotoxicity of selected chemotherapeutic agents. ** Sup-T1… **Fig. 3.. PIP4K2A knockdown is primarily responsible for enhanced cytotoxicity of selected chemotherapeutic agents.** Sup-T1 cells expressing doxycycline-inducible shRNAs targeting PIP4K2A/2B (**A**), PIP4K2A (**B**), or PIP4K2B (**C**) were treated with dexamethasone (Dex), doxorubicin (Doxo), etoposide (Eto), or _L_ -asparaginase (L-Asp) at fixed concentrations (Dex, 20 nM; Doxo, 500 nM; Eto, μ3 M; L-Asp, 5 μg/ml). Cell proliferation was measured and expressed as a percentage of control cells in the absence of drug (DMSO). Open bars indicate −DOX, and gray bars indicate +DOX. Data are presented as mean ± SEM (n = 3). Statistical significance was determined using Student’s _t_ -test; ***_P_ < 0.0001; **_P_ < 0.001; *_P_ < 0.01. [ ![Fig. 4.](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc2a/13528604/8f9ad01b3b77/nihms-2203602-f0004.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc2a/13528604/61bdfa94e842/nihms-2203602-f0004.webp) ** Fig. 4.. Pharmacological inhibition of PIP4K2A does… ** ** Fig. 4.. Pharmacological inhibition of PIP4K2A does not affect Sup-T1 cell proliferation, nelarabine sensitivity, or… ** **Fig. 4.. Pharmacological inhibition of PIP4K2A does not affect Sup-T1 cell proliferation, nelarabine sensitivity, or AKT phosphorylation.** **A.** Parent Sup-T1 cells were treated with the PIP4K inhibitors 066ATZ or BAY-091, and effects on proliferation, drug response, and signaling were assessed. Top left: Dose–response of 066ATZ showing no significant effect on cell proliferation. Top right: Dose–response curves for nelarabine in the presence of DMSO (solid line) or 20 μM 066ATZ (dashed line). Middle left: Dose–response of BAY-091 showing no significant effect on cell proliferation. Middle right: Dose–response curves for nelarabine in the presence of DMSO (solid line) or 10 μM BAY-091 (dashed line). Cell proliferation in all panels is expressed as a percentage of control cells in the absence of drug. Bottom: Immunoblot analysis of phosphorylated AKT showing no detectable change following treatment with 066ATZ or BAY-091. **B.** Sup-T1 cells expressing a doxycycline-inducible shRNA targeting PIP4K2B were treated with doxycycline and exposed to the PIP4K inhibitors 066ATZ or BAY-091. Effects on proliferation, drug response, and AKT signaling were assessed as in Fig. 4A. [See this image and copyright information in PMC](https://pubmed.ncbi.nlm.nih.gov/42570494/) ## Similar articles * [ Selective induction of apoptosis in T-cell acute lymphoblastic leukemia by pristimerin through dual PI3K/AKT pathway inhibition and ROS generation. ](https://pubmed.ncbi.nlm.nih.gov/41202965/) Kuttikrishnan S, Mariyam Z, Ahmad F, Suleman M, Habeeba U, Panicker AJ, Prabhu KS, Merhi M, Dermime S, Al Shabeeb Akil AS, Bhat AA, Ansari AW, Uddin S.Kuttikrishnan S, et al.Eur J Pharmacol. 2025 Dec 5;1008:178329. doi: 10.1016/j.ejphar.2025.178329. Epub 2025 Nov 5.Eur J Pharmacol. 2025.PMID: 41202965 * [ Sphingosine kinase 1 counteracts chemosensitivity and immune evasion in diffuse large B cell lymphoma cells via the PI3K/AKT/PD-L1 axis. ](https://pubmed.ncbi.nlm.nih.gov/39418735/) Liu D, Liu L, Li H, Huang Z, Wang Y.Liu D, et al.Int Immunopharmacol. 2024 Dec 25;143(Pt 2):113361. doi: 10.1016/j.intimp.2024.113361. 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