cervical-cancer

HPV's cancer-causing protein has an additional mechanism for promoting cervical cancer progression

Human papillomavirus (HPV) causes cervical cancer mainly through its E7 oncoprotein, which disables the tumor suppressor Rb. Previous research showed E7 can increase levels of LASP1 — a protein that promotes cancer cell proliferation and invasion — by suppressing a microRNA that normally limits…

Dan Manning

Dan Manning

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HPV's cancer-causing protein has an additional mechanism for promoting cervical cancer progression

HPV's cancer-causing protein has an additional mechanism for promoting cervical cancer progression

Human papillomavirus (HPV) causes cervical cancer mainly through its E7 oncoprotein, which disables the tumor suppressor Rb. Previous research showed E7 can increase levels of LASP1 — a protein that promotes cancer cell proliferation and invasion — by suppressing a microRNA that normally limits LASP1 expression.

This study identifies a second, additional mechanism: E7 also activates LASP1 transcription directly through the Rb/E2F1 signaling pathway. By inactivating Rb, E7 frees E2F1 to activate LASP1 gene transcription directly. This means HPV uses at least two distinct molecular routes to elevate LASP1 in cervical cancer cells.

Understanding multiple regulatory mechanisms for LASP1 could identify new points of therapeutic intervention in HPV-positive cervical cancers, particularly given that LASP1 promotes the invasive behaviors that lead to metastasis.

Key Findings

  • HPV E7 oncoprotein activates LASP1 transcription via the Rb/E2F1 signaling pathway
  • This represents a second mechanism (alongside microRNA suppression) by which E7 elevates LASP1
  • Rb/E2F1 pathway activation by E7 is a key driver of LASP1 expression in HPV+ cervical cancer
  • LASP1 promotes cell proliferation and invasion in HPV-positive cervical cancer cells
  • Multiple convergent pathways elevate LASP1 in HPV-driven cervical cancer

Implications

These findings deepen our understanding of how HPV drives cervical cancer progression through LASP1 and may identify new therapeutic targets. LASP1 inhibition or targeting E2F1 activity could be strategies worth exploring in HPV-positive cervical cancer patients.

Caveats

Preprint, not peer reviewed. Study is likely cell-line based; clinical validation in patient tumors is needed. The functional importance of this specific E7-Rb-E2F1-LASP1 axis relative to other E7 oncogenic functions remains to be fully characterized. Summary based on abstract only.

Source: bioRxiv — 2026-04-10

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